成功大學博碩士論文系統

簡易檢索 / 詳目顯示

回結果列表

研究生：	陳子豪 Chen, Tzu-Hao
論文名稱：	一氧化碳中毒驅動之肺-腸軸:由肺泡-微血管屏障損傷到腸道屏障破壞與全身性發炎的整合性證據 Carbon monoxide poisoning drives a lung-gut axis: integrating alveolar-capillary barrier injury, intestinal barrier breakdown, and systemic inflammation
指導教授：	王應然 Wang, Ying-Jan
共同指導:	黃建程 Huang, Chien-Cheng
學位類別：	博士 Doctor
系所名稱：	醫學院 - 環境醫學研究所 Department of Environmental and Occupational Health
論文出版年：	2026
畢業學年度：	114
語文別：	英文
論文頁數：	146
中文關鍵詞：	一氧化碳中毒、肺–腸軸線、屏障功能失調、全身性發炎、慢性阻塞性肺病、腸道菌相失衡、免疫代謝失調、高壓氧治療
外文關鍵詞：	Carbon monoxide poisoning, lung-gut axis, barrier dysfunction, systemic inflammation, COPD, gut microbiota dysbiosis, immunometabolic dysregulation, hyperbaric oxygen therapy
相關次數：	點閱：29 下載：0
分享至:	分享至facebook 分享至twitter

查詢本校圖書館目錄查詢臺灣博碩士論文知識加值系統勘誤回報

一氧化碳中毒（carbon monoxide poisoning, COP）傳統上被視為一種急性缺氧性傷害；然而，日益累積的臨床觀察與長期追蹤證據顯示，倖存者可能在暴露後發展出延遲性且涉及多器官的後遺症。本論文聚焦於肺臟與腸道，原因在於兩者為人體與外在環境接觸的最大屏障介面，且共享一致的易感性結構，包括共同的上游致病因子（CO 所致的全身性低氧）、共同的核心受損標的（上皮–微血管單元），以及共同的下游結果（屏障破壞與白血球募集）。這些共享特徵亦形成一套共同的傷害放大邏輯，使循環中的發炎訊號與內皮破壞因子得以跨器官傳播並加劇病理傷害。基於此，本論文建立並驗證 COP 所驅動之「肺–腸軸線」作為一個整合性的病理生物學連續體。
本論文的整體目標在於透過結合族群流行病學證據與動物模式的因果驗證，釐清 COP 後肺–腸軸線在長期臨床後果中的角色及其分子機轉。本研究整合兩篇已發表於 Environmental Pollution 與 Life Sciences 的轉譯醫學研究，兩項研究皆採用雙重證據策略：（一）全國性世代研究以量化 COP 後的長期疾病風險；（二）大鼠 COP 模式以探討組織、細胞及分子層級的致病機制。
在以肺臟為核心的研究中，流行病學分析顯示 COP 病患具有較高的慢性阻塞性肺病（chronic obstructive pulmonary disease, COPD）發生風險。在動物實驗中，CO 暴露成功重現 COPD 樣病理特徵，包括類肺氣腫的結構破壞，以及伴隨免疫失衡的持續性細胞激素相關發炎反應。支氣管肺泡灌洗液與肺實質中可觀察到顯著的免疫細胞浸潤，包含巨噬細胞極化特徵與伴隨細胞激素共表現的嗜中性球募集。其關鍵機轉特徵為肺泡屏障受損，表現為緊密連結蛋白下降，以及肺泡第二型上皮細胞中的粒線體壓力反應。此粒線體壓力進一步導致粒線體動態失衡、Pink1/Parkin 介導之粒線體自噬活化，以及細胞程式性死亡途徑（焦亡與凋亡）的啟動，最終造成 COPD 樣的生理功能異常。值得注意的是，高壓氧治療（hyperbaric oxygen therapy, HBOT）可顯著改善肺部病理變化與功能表現，並伴隨粒線體恆定性恢復、細胞死亡訊號抑制及發炎反應減弱，顯示粒線體品質控制與屏障維持為 COP 相關慢性肺損傷之可介入治療標的。
在以腸道為核心的研究中，利用台灣全民健康保險研究資料庫的全國性世代分析顯示，COP 與多種腸道疾病的長期發生風險顯著增加。機轉上，大鼠 COP 模式顯示多節段性腸道損傷（尤以十二指腸與空腸為著），伴隨腸道通透性上升與緊密連結結構受損，並同時出現全身性發炎特徵與免疫活化反應。此外，COP 亦造成免疫–代謝恆定性的耦合性失衡，表現為腸胃道與壓力／代謝相關荷爾蒙異常、血糖與脂質指標上升，以及腸道菌相失衡，整體連結了上皮屏障破壞與菌相–代謝–免疫失調之病理軸線。
綜合上述證據，本論文將 COP 界定為一種以屏障破壞為核心的全身性發炎疾病，而非侷限於單一器官的病變，並提出一個整合性的肺–腸軸線模型。具體而言，COP 所誘發的肺泡屏障受損與粒線體壓力可產生循環性的發炎與內皮破壞訊號，進而促發腸道屏障崩解與菌相相關的免疫–代謝失衡；反之，腸道來源的發炎與免疫代謝擾動亦可能回饋性地維持並放大肺部發炎反應，形成自我增強的惡性循環。在概念層面上，本研究以共同的上游致病因子與共享的屏障標的為基礎，整合 COP 後多器官後遺症於一致的機轉架構中；在方法學上，證實結合全國性流行病學推論與動物模式因果驗證，有助於由相關性推進至生物學合理性；在轉譯層面上，本研究支持 HBOT 作為具機轉基礎的治療策略，並進一步指出同時鎖定粒線體品質控制與屏障維持之機轉導向介入，可能中斷肺–腸軸線的病理放大循環，從而將 COP 後的臨床後果重新定位為一種可被機轉導向治療的、以屏障為核心的全身性發炎連續體。

Carbon monoxide poisoning (COP) is classically regarded as an acute hypoxic insult; however, converging clinical observations and longitudinal evidence indicate that survivors may develop delayed, multi-organ sequelae. This dissertation focuses on the lung and gut because they are the body’s two largest barrier interfaces with the external environment and share a coherent vulnerability architecture: a common upstream driver (CO-induced systemic hypoxemia), a common core target (the epithelial-microvascular unit), and common downstream consequences (barrier disruption and leukocyte recruitment). These shared features also enable a common amplification logic, whereby circulating inflammatory and endothelial-disruptive cues propagate injury across organs. On this basis, this dissertation establishes and substantiates a COP-driven lung-gut axis as a unifying pathobiological continuum.
The overarching objective of this dissertation was to define the long-term clinical relevance and mechanistic underpinnings of a lung-gut axis following COP by triangulating population-based epidemiology with causal validation in animal models. To accomplish this, the dissertation integrates two complementary peer-reviewed translational studies published in Environmental Pollution and Life Sciences. Both studies were designed with a dual-evidence strategy: (i) nationwide cohort analyses to quantify long-term disease associations after COP, and (ii) rat COP models to interrogate tissue-, cellular-, and molecular-level mechanisms.
In the lung-focused study, epidemiological analysis demonstrated that COP patients are associated with an increased risk of chronic obstructive pulmonary disease (COPD). In rats, CO exposure reproduced key COPD-like features, including emphysema-like structural derangement and persistent cytokine-linked inflammation with immune dysregulation. Immune-cell infiltration was observed in bronchoalveolar lavage fluid and lung parenchyma, including macrophage polarization signatures and neutrophil recruitment with cytokine co-expression. A defining mechanistic signature was alveolar barrier compromise, evidenced by decreased tight junction proteins, along with mitochondrial stress in alveolar type II cells. This mitochondrial stress manifested as dysregulated mitochondrial dynamics, activation of Pink1/Parkin-mediated mitophagy, and engagement of programmed cell-death pathways (pyroptosis and apoptosis), culminating in COPD-like physiological abnormalities. Importantly, hyperbaric oxygen therapy (HBOT) mitigated lung pathology and improved functional outcomes, concomitant with restoration of mitochondrial homeostasis, suppression of cell-death signaling, and attenuation of inflammatory activation—thereby identifying mitochondrial quality control and barrier preservation as actionable therapeutic targets in COP-related chronic lung injury.
In the gut-focused study, a nationwide cohort analysis using Taiwan’s National Health Insurance Research Database demonstrated that COP is associated with an increased long-term risk of intestinal diseases. Mechanistically, a rat COP model revealed multi-segment intestinal injury (notably in the duodenum and jejunum), increased intestinal permeability, and impaired tight-junction integrity, accompanied by systemic inflammatory signatures and immune activation. COP also induced a coupled disruption of immunometabolic homeostasis, reflected by alterations in gastrointestinal and stress/metabolic hormones, elevations in glucose and lipid indices, and gut microbiota dysbiosis, collectively linking epithelial barrier failure to microbiota-metabolic-immune imbalance.
Synthesizing both lines of evidence, this dissertation defines COP as a barrier-centered systemic inflammatory disorder that extends beyond isolated organ pathology and proposes an integrated lung-gut axis model. Specifically, COP-triggered alveolar barrier compromise coupled with mitochondrial stress generates circulating inflammatory and endothelial-disruptive cues that plausibly predispose to intestinal barrier breakdown and microbiota-linked immunometabolic derangements; reciprocally, gut-associated inflammatory and immunometabolic perturbations may feed back to sustain and amplify pulmonary inflammation, establishing a self-reinforcing loop. Conceptually, this work unifies post-COP sequelae within a coherent mechanistic framework anchored in shared upstream drivers and shared barrier targets. Methodologically, it demonstrates the value of triangulating nationwide epidemiological inference with mechanistic animal validation to move from association to biological plausibility. Translationally, it supports HBOT as a mechanistically grounded therapeutic strategy while motivating future mechanism-guided interventions that co-target mitochondrial quality control and barrier preservation as actionable therapeutic targets to interrupt the lung-gut amplification cycle, thereby reframing post-COP outcomes from organ-specific complications to a unified, barrier-centered, systemic inflammatory continuum that is amenable to mechanism-guided intervention.

中文摘要 3
Abstract 5
致謝 8
1. Introduction 15
1.1. Main 15
1.2. The mechanism of CO intoxication 15
1.3. CO-induced pulmonary and intestinal diseases 16
1.4. A variety of different cell death pathways, including pyroptosis, mitophagy, and apoptosis related to mitochondrial dysfunction after COP 18
1.5. Hyperbaric oxygen therapy (HBOT) for COP 19
1.6. The possible mechanism linking the lung-gut axis after COP 21
1.7. Overall hypothesis 23
2. Material and Methods 25
2.1. Epidemiologic study data source 25
2.2. COP cohort and non-COP cohort related to COPD 25
2.3. Variable definitions 26
2.4. Outcome measurements 26
2.5. Epidemiology and animal ethical statements	27
2.6. Animal 27
2.7. COP experimental rat model	28
2.8. Intermittent hyperbaric oxygen therapy 28
2.9. Cytoarchitecture changes by H&E stain 29
2.10. Multi-cytokines and chemokines expression in the BALF and serum 29
2.11. Flow cytometry analysis 30
2.12. Immunofluorescence (IF) staining 30
2.13. Western blot 31
2.14. Enzyme-linked immunosorbent assay (ELISA)	31
2.15. Assessment of gut-derived metabolic hormones 32
2.16. Transmission electron microscope (TEM) with immunogold labelling analysis of the lung tissue 32
2.17. Measurement of lung physiology and function 33
2.18. Intestinal integrity assessment 34
2.19. Extraction of bacterial DNA from feces 35
2.20. Microbiome bioinformatics analysis 35
2.21. Sample size calculation of animal study 37
2.22. Statistical analysis 38
3. Results	39
3.1. Part I: CO intoxication induce pulmonary injury 40
3.1.1. Cytoarchitecture change in the lung after COP 40
3.1.2. CO increased lung permeability via disrupting tight junction protein 40
3.1.3. Hyperinflammation existed after CO intoxication 41
3.1.3.1. Plenty of pro-inflammatory medicators were detected in the lung after COP 41
3.1.3.2. Dysregulation immune burden in the lung after COP 42
3.1.4.	The categories of mediators secreted by different somatic and/or immune cells under after COP 42
3.1.4.1. Cytokine and chemokine secretion in AT-I cells	43
3.1.4.2. Cytokine and chemokine secretion in AT-II cells 43
3.1.4.3. Cytokine and chemokine secretion in CD86+ macrophages 44
3.1.4.4. Cytokine and chemokine secretion in neutrophils 44
3.1.5. COP induces mitochondrial structural damage and shifts mitochondrial dynamics toward fission dominance in AT-II cells 45
3.1.6. COP provokes mitophagy, inflammasome-mediated pyroptosis, and intrinsic apoptosis in lung tissue	46
3.1.7. COP deteriorated lung function and may be developed to COPD-like features 48
3.1.8. Population-based evidence indicates an elevated incidence of COPD following COP	49
3.1.9. Mini-summary of pulmonary-related research under COP 50
3.2. CO exposure provokes gastrointestinal pathology 51
3.2.1. Structural damage of the intestine and disruption of gut-derived hormonal balance 51
3.2.2. Systemic immune activation and cytokine surge following CO exposure 52
3.2.3. Breakdown of intestinal and vascular barriers after carbon monoxide intoxication	53
3.2.4. CO exposure reshapes gut microbial ecology 54
3.2.4.1. Alterations in microbial composition and community structure 54
3.2.4.2. Identification of discriminative microbial taxa associated with COP 54
3.2.4.3. Functional reprogramming of gut microbiota predicted by KEGG pathways 55
3.2.5. Associations between gut microbes, inflammatory mediators, and metabolic disruption 55
3.2.6. Population-based confirmation of elevated intestinal disease risk following COP 56
3.2.7. Mini-summary of intestinal-related research under COP 58
4. Discussion 59
4.1. Main Finding 59
4.2. Protocol heterogeneity in acute COP models and the justification for a symptom-aligned exposure regimen 59
4.3. CO as more than a toxicant: an environmental contaminant posing acute and long-term threats 60
4.4. Differential intestinal susceptibility following COP: epidemiological evidence highlights age- and sex-related disparities	62
4.5. COP caused clinically concordant pulmonary injury and significantly increased the risk of developing COPD 63
4.6. Impaired mitochondrial homeostasis as a central mechanism contributed to various cell death pathways in CO-induced lung injury 65
4.7. Immune/Inflammation regulation upon COP 67
4.8. Excessive inflammatory activation may originate from COP-driven microbial imbalance and disrupted metabolic hormone signaling 69
4.9. Microbial communities and their metabolites as contributors to metabolic dysfunction 71
4.10. Alterations in the gut–brain axis following COP 71
4.11. The Lung-gut axis following COP 72
4.11.1. Immune and inflammatory interactions along the lung–gut axis 73
4.11.2. Gut-derived metabolites as modulators of pulmonary injury 73
4.11.3. Renin–angiotensin system and peroxisome proliferator-activated receptors (PPARs) immunometabolic disruption 74
4.11.4.	Upregulation of glycerophospholipid metabolism as an adaptive lipid remodeling mechanism along the lung–gut axis following COP	75
4.11.5.	Downregulation of sphingolipid metabolism as a protective suppression of pro‑inflammatory lipid signaling along the lung–gut axis following COP	76
4.12. HBOT and the translational applications of the current study 78
5. Limitations and future directions 81
6. Conclusion 83
7. References 84
8. Table 100
Table 1. The detailed information on conjugated fluorescence antibody for flow cytometry. 100
Table 2. The detailed information on primary and secondary antibodies with respective dilutions for immunofluorescence approaches. 101
Table 3. The detailed information on primary and secondary antibodies with respective dilutions for Western blot determinations. 102
Table 4. The detailed information on ELISA. 104
Table 5. Comparison of age, sex, lifestyle, and underlying comorbidities between COP cohort and non-COP cohort in the COPD study. 105
Table 6. Comparison of the risk for developing COPD between COP cohort and non-COP cohort by competing risk analysis. 106
Table 7. Independent predictors of COPD in all participants by a multivariable Cox. 108
Table 8. Comparison of demographic characteristics and underlying comorbidities between COP and non-COP cohorts in the intestinal study. 109
Table 9. Comparison of the risk for intestinal diseases between COP and non-COP cohorts by Cox proportional hazard regression analysis. 110
Table 10. Independent predictors of intestinal diseases in all participants by a Cox proportional hazard regression analysis. 112
Table 11. Summarized real-world environmental and occupational CO exposure levels. 113
9. Figures and figure legends 114
Figure 1. The multi-histopathological features and tight junction proteins expression in the lung after COP. 114
Figure 2. The levels of various cytokines and chemokines, along with cytological analysis, showed an increase following COP. 116
Figure 3. The categories of mediators secreted by AT-I cells under CO intoxication. 118
Figure 4. The categories of mediators secreted by AT-II cells under CO intoxication. 119
Figure 5. The categories of mediators secreted by CD86+ macrophages during CO intoxication. 120
Figure 6. The categories of mediators secreted by neutrophils during CO intoxication. 121
Figure 7.  Illustration diagram of a summarized cytokines expression in multiple cell types of the lung on the 28th day of COP. 122
Figure 8. Changes in the morphology of mitochondria and lamellar bodies and an imbalance of mitochondrial fusion and fission in lung AT-II cells after COP. 123
Figure 9. Disrupted mitochondria triggered Pink1/Parkin-mediated mitophagy, NLRP3 inflammasome-mediated pyroptosis, and intrinsic apoptosis. 125
Figure 10. COPD-like physiological lung function changes 28 and 56 days after COP, while HBOT had a therapeutic effect on reversing deficits. 127
Figure 11. Comparison of COPD risk between the COP cohort and non-COP cohort using Kaplan‒Meier curves according to 14-year follow-up data. 129
Figure 12. Graphic summary of pulmonary-related research under COP. 130
Figure 13. Histopathological features of the intestine and relative metabolic hormone expression after COP. 132
Figure 14. COP induced a high expression of cytokines and chemokines, along with pro-inflammatory immune cells. 133
Figure 15. COP induced intestinal barrier dysfunction and hyperpermeability. 134
Figure 16. COP changed intestinal microbiota composition and abundance and was linked to dysregulated metabolic pathways. 135
Figure 17. Correlation analysis of inflammatory cytokines/chemokines with specific microbiota taxa and biological function assessment regarding lipid metabolism and metabolic disease. 137
Figure 18. Comparison of the risk for intestinal diseases between patients with COP and non-COP cohort by Kaplan–Meier’s method and log-rank test. 138
Figure 19. Graphic summary of intestinal-related research under COP. 139
10. Supplementary figure legends 140
Figure S1. Representative images from the lung parenchyma to the panoramic view of the pulmonary lobe superior to the left lung. 140
Figure S2. Selective cytokines/chemokines determination by relative ELISAs. 141
Figure S3. Detailed flow cytometry gating analysis for distinct cell types after day 3 of CO poisoning. 143
Figure S4. Detailed flow cytometry gating analysis for distinct cell types after day 28 of CO poisoning. 145
Figure S5. The lungs manifested emphysema-like features after CO exposure, as indicated by an increasing mean linear intercept (MLI). 146
                                    

1. Prockop, L.D. and R.I. Chichkova, Carbon monoxide intoxication: an updated review. J Neurol Sci, 2007. 262(1-2): p. 122-30.
2. Emmanuel, B., Determination of Carbon Monoxide Concentration in Industrial and Commercial Areas of Kano Metropolis, Kano State, Nigeria. World Environment, 2013. 3(4): p. 133-137.
3. Idriss, U. and A. Muhammad, Assessment and Monitoring of Carbon Monoxide (CO) Concentrations in High Traffic Areas (HTA) of Maiduguri Metropolitan of Borno State, Nigeria. European Journal of Environment and Earth Sciences, 2021. 2: p. 63-66.
4. Moges, G.T. and G.T. Alemu, Contribution of congested traffic flow condition to air pollution at intersections in Addis Ababa, Ethiopia. Heliyon, 2024. 10(17): p. e36477.
5. Woolley, K., et al., Biomass cooking carbon monoxide levels in commercial canteens in Kigali, Rwanda. Arch Environ Occup Health, 2021. 76(2): p. 75-85.
6. Pan, K.T., et al., Can Exhaled Carbon Monoxide Be Used as a Marker of Exposure? A Cross-Sectional Study in Young Adults. Int J Environ Res Public Health, 2021. 18(22).
7. Semmens, E.O., et al., Carbon monoxide exposures in wildland firefighters in the United States and targets for exposure reduction. J Expo Sci Environ Epidemiol, 2021. 31(5): p. 923-929.
8. Bruce, N., R. Perez-Padilla, and R. Albalak, Indoor air pollution in developing countries: a major environmental and public health challenge. Bull World Health Organ, 2000. 78(9): p. 1078-92.
9. Teleszewski, T.J. and K. Gładyszewska-Fiedoruk, Carbon Monoxide Concentration in the Garage of a Single-Family House—Experiment and One-Dimensional Model of Carbon Monoxide Concentration. Applied Sciences, 2025. 15(3): p. 1146.
10. Wang, Z., et al., Numerical Simulation of the Ventilation and Fire Conditions in an Underground Garage with an Induced Ventilation System. Buildings, 2023. 13(8): p. 2074.
11. Grieb, G., et al., Glasgow Coma Scale and laboratory markers are superior to COHb in predicting CO intoxication severity. Burns, 2011. 37(4): p. 610-5.
12. Huang, C.C., et al., Exposure Duration and History of Hypertension Predicted Neurological Sequelae in Patients with Carbon Monoxide Poisoning. Epidemiology, 2019. 30 Suppl 1: p. S76-S81.
13. Ku, C.H., et al., Outcome of patients with carbon monoxide poisoning at a far-east poison center. PLoS One, 2015. 10(3): p. e0118995.
14. Huang, C.C., et al., Long-term prognosis of patients with carbon monoxide poisoning: a nationwide cohort study. PLoS One, 2014. 9(8): p. e105503.
15. Rose, J.J., et al., Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy. Am J Respir Crit Care Med, 2017. 195(5): p. 596-606.
16. Jang, D.H., et al., Emerging cellular-based therapies in carbon monoxide poisoning. Am J Physiol Cell Physiol, 2021. 321(2): p. C269-C275.
17. Hampson, N.B., et al., Practice recommendations in the diagnosis, management, and prevention of carbon monoxide poisoning. Am J Respir Crit Care Med, 2012. 186(11): p. 1095-101.
18. Weaver, L.K., Clinical practice. Carbon monoxide poisoning. N Engl J Med, 2009. 360(12): p. 1217-25.
19. Huang, C.-C., et al., Association between carbon monoxide poisoning and adrenal insufficienc y: a nationwide cohort study. Scientific reports. 12(1): p. 16219.
20. Huang, C.-C., et al., Autoimmune Connective Tissue Disease Following Carbon Monoxide Poisoni ng: A Nationwide Population-Based Cohort Study. Clin. Epidemiol. . 12: p. 1287-1298.
21. Huang, C.-C., et al., Increased Risk of Congestive Heart Failure Following Carbon Monoxide P oisoning. Circulation. Heart failure. 14(4): p. e007267.
22. Huang, C.-C., et al., Risks of Developing Diabetes and Hyperglycemic Crisis Following Carbon Monoxide Poisoning: A Study Incorporating Epidemiologic Analysis and Animal Experiment. Clinical epidemiology. 14: p. 1265-1279.
23. Huang, C.-C., et al., Risk of Myocardial Infarction After Carbon Monoxide Poisoning: A Natio nwide Population-Based Cohort Study. Cardiovasc. Toxicol. 19(2): p. 147-155.
24. Huang, C.-C., et al., Increased risk for hypothyroidism associated with carbon monoxide pois oning: a nationwide population-based cohort study. Sci. Rep. 9(1): p. 16512.
25. Chen, R.J., et al., Carbon monoxide-triggered health effects: the important role of the inflammasome and its possible crosstalk with autophagy and exosomes. Arch Toxicol, 2021. 95(4): p. 1141-1159.
26. Pehlivan S¹*, A.H., Samdanci E³, Kara D¹, Turkkan D¹, Altuntas A4, Gurler M² and Karapirli M5**, Evaluation of Lung, Cardiac and Brain Pathologies of Death Cases Caused by Carbon Monoxide Poisoning. Austin J Clin Neurol 2016. 3(1).
27. Niden, A.H. and H. Schulz, The ultrastructural effects of carbon monoxide inhalation on the rat lung. Virchows Arch Pathol Anat Physiol Klin Med, 1965. 339(4): p. 283-92.
28. Schneir, A. and L. Rentmeester, Carbon monoxide poisoning and pulmonary injury from the mixture of formic and sulfuric acids. Clin Toxicol (Phila), 2016. 54(5): p. 450-3.
29. Tan CY, Y.S., Chua YX., Unusual delayed pulmonary presentation of carbon monoxide poisoning: a case report. . Clin Case Rep J, 2022. 3(2): p. 1-4.
30. Song, J., et al., Association of ambient carbon monoxide exposure with hospitalization risk for respiratory diseases: A time series study in Ganzhou, China. Front Public Health, 2023. 11: p. 1106336.
31. Lee, S.J., et al., Risk of lung diseases in patients with previous carbon monoxide poisoning: a nationwide population-based cohort study in the Republic of Korea. Clin Toxicol (Phila), 2024. 62(7): p. 425-431.
32. Roderique, J.D., et al., A modern literature review of carbon monoxide poisoning theories, therapies, and potential targets for therapy advancement. Toxicology, 2015. 334: p. 45-58.
33. Liu, Y., et al., Ambient carbon monoxide and relative risk of daily hospital outpatient visits for respiratory diseases in Lanzhou, China. Int J Biometeorol, 2023. 67(12): p. 1913-1925.
34. Brusselle, G.G., G.F. Joos, and K.R. Bracke, New insights into the immunology of chronic obstructive pulmonary disease. Lancet, 2011. 378(9795): p. 1015-26.
35. Arora, S., et al., Macrophages: Their role, activation and polarization in pulmonary diseases. Immunobiology, 2018. 223(4-5): p. 383-396.
36. Barnes, P.J., Inflammatory mechanisms in patients with chronic obstructive pulmonary disease. J Allergy Clin Immunol, 2016. 138(1): p. 16-27.
37. Fan, Y. and O. Pedersen, Gut microbiota in human metabolic health and disease. Nat Rev Microbiol, 2021. 19(1): p. 55-71.
38. Akyol, S., et al., The role of reactive oxygen species and oxidative stress in carbon monoxide toxicity: an in-depth analysis. Redox Rep, 2014. 19(5): p. 180-9.
39. Gokdemir, G.S., et al., Effects of acute carbon monoxide poisoning on liver damage and comparisons of related oxygen therapies in a rat model. Toxicol Mech Methods, 2024. 34(8): p. 845-854.
40. Li, J., et al., Involvement of p38 mitogen-activated protein kinase in altered expressions of AQP1 and AQP4 after carbon monoxide poisoning in rat astrocytes. Basic Clin Pharmacol Toxicol, 2019. 125(4): p. 394-404.
41. Pang, L., et al., Erythropoietin Protects Rat Brain Injury from Carbon Monoxide Poisoning by Inhibiting Toll-Like Receptor 4/NF-kappa B-Dependent Inflammatory Responses. Inflammation, 2016. 39(2): p. 561-8.
42. Xiong, K., et al., Dysfunction of the Gut-Brain-Axis in delayed encephalopathy after carbon monoxide poisoning. Medical Hypotheses, 2025. 195: p. 111550.
43. Ghosh, S.S., et al., Intestinal Barrier Dysfunction, LPS Translocation, and Disease Development. J Endocr Soc, 2020. 4(2): p. bvz039.
44. Winer, D.A., et al., The Intestinal Immune System in Obesity and Insulin Resistance. Cell Metab, 2016. 23(3): p. 413-26.
45. Miner-Williams, W.M. and P.J. Moughan, Intestinal barrier dysfunction: implications for chronic inflammatory conditions of the bowel. Nutr Res Rev, 2016. 29(1): p. 40-59.
46. Yang, G., et al., Role of the gut microbiota in type 2 diabetes and related diseases. Metabolism, 2021. 117: p. 154712.
47. Huang, C.C., et al., Risks of Developing Diabetes and Hyperglycemic Crisis Following Carbon Monoxide Poisoning: A Study Incorporating Epidemiologic Analysis and Animal Experiment. Clin Epidemiol, 2022. 14: p. 1265-1279.
48. Feng, Y., et al., Pyroptosis in inflammation-related respiratory disease. J Physiol Biochem, 2022. 78(4): p. 721-737.
49. Koranteng, J., et al., The role of mitochondria in eosinophil function: implications for severe asthma pathogenesis. Front Cell Dev Biol, 2024. 12: p. 1360079.
50. Liu, J., et al., Mitochondrial quality control in lung diseases: current research and future directions. Front Physiol, 2023. 14: p. 1236651.
51. Sharma, A., et al., Mitochondrial dynamics and mitophagy in lung disorders. Life Sci, 2021. 284: p. 119876.
52. Huang, W.H., et al., Resveratrol Attenuates Inflammation in Acute Lung Injury through ROS-Triggered TXNIP/NLRP3 Pathway. Chin J Integr Med, 2025.
53. Chang, T.M., et al., Promotion of ROS-mediated apoptosis, G2/M arrest, and autophagy by naringenin in non-small cell lung cancer. Int J Biol Sci, 2024. 20(3): p. 1093-1109.
54. Tian, L., et al., Ambient ozone exposure induces ROS related-mitophagy and pyroptosis via NLRP3 inflammasome activation in rat lung cells. Ecotoxicol Environ Saf, 2022. 240: p. 113663.
55. Weaver, L.K., et al., Carboxyhemoglobin half-life in carbon monoxide-poisoned patients treated with 100% oxygen at atmospheric pressure. Chest, 2000. 117(3): p. 801-8.
56. Thom, S.R., Hyperbaric oxygen: its mechanisms and efficacy. Plast Reconstr Surg, 2011. 127 Suppl 1(Suppl 1): p. 131S-141S.
57. Undersea, H.M.S.H.O. Committee, and L.K. Weaver, Hyperbaric Oxygen Therapy Indications: The Hyperbaric Oxygen Therapy Committee Report. 2014: Best Publishing Company.
58. Schottlender, N., I. Gottfried, and U. Ashery, Hyperbaric Oxygen Treatment: Effects on Mitochondrial Function and Oxidative Stress. Biomolecules, 2021. 11(12).
59. Garrabou, G., et al., Mitochondrial injury in human acute carbon monoxide poisoning: the effect of oxygen treatment. J Environ Sci Health C Environ Carcinog Ecotoxicol Rev, 2011. 29(1): p. 32-51.
60. Weaver, L.K., et al., Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med, 2002. 347(14): p. 1057-67.
61. Wada, K., et al., Repeated hyperbaric oxygen induces ischemic tolerance in gerbil hippocampus. Brain Res, 1996. 740(1-2): p. 15-20.
62. Fu, Q., et al., Hyperbaric oxygen therapy for healthy aging: From mechanisms to therapeutics. Redox Biol, 2022. 53: p. 102352.
63. Arya, A.K., et al., Inflammatory responses to acute carbon monoxide poisoning and the role of plasma gelsolin. Sci Adv, 2025. 11(6): p. eado9751.
64. Ziaka, M. and A. Exadaktylos, Gut-derived immune cells and the gut-lung axis in ARDS. Crit Care, 2024. 28(1): p. 220.
65. Kuriiwa, F., et al., Mitochondrial toxins potentiate hydroxyl radical production in rat striatum during carbon monoxide poisoning. J Pharmacol Sci, 2021. 146(1): p. 29-32.
66. Xu, R., et al., Immunometabolism: signaling pathways, homeostasis, and therapeutic targets. MedComm (2020), 2024. 5(11): p. e789.
67. Chakraborty, S., J. Pramanik, and B. Mahata, Revisiting steroidogenesis and its role in immune regulation with the advanced tools and technologies. Genes Immun, 2021. 22(3): p. 125-140.
68. Goss, V., A.N. Hunt, and A.D. Postle, Regulation of lung surfactant phospholipid synthesis and metabolism. Biochim Biophys Acta, 2013. 1831(2): p. 448-58.
69. Liu, M., et al., Hyperbaric oxygen treatment mitigates gut dysbiosis of mice with spinal cord injury. J Mol Med (Berl), 2025. 103(11-12): p. 1515-1532.
70. Lin, L.Y., et al., Data resource profile: the National Health Insurance Research Database (NHIRD). Epidemiol Health, 2018. 40: p. e2018062.
71. Hsieh, C.Y., et al., Taiwan's National Health Insurance Research Database: past and future. Clin Epidemiol, 2019. 11: p. 349-358.
72. Huang, C.C., et al., Increased Risk of Congestive Heart Failure Following Carbon Monoxide Poisoning. Circ Heart Fail, 2021. 14(4): p. e007267.
73. Huang, C.C., et al., Impact of Hyperbaric Oxygen Therapy on Subsequent Neurological Sequelae Following Carbon Monoxide Poisoning. J Clin Med, 2018. 7(10).
74. Huang, C.C., et al., Hyperbaric Oxygen Therapy Is Associated With Lower Short- and Long-Term Mortality in Patients With Carbon Monoxide Poisoning. Chest, 2017. 152(5): p. 943-953.
75. Myasoedova, E., et al., Prevalence and risk factors of gastrointestinal disorders in patients with rheumatoid arthritis: results from a population-based survey in olmsted county, Minnesota. Gastroenterol Res Pract, 2011. 2011: p. 745829.
76. Fan, D.F., et al., Neuroprotective effects of exogenous methane in a rat model of acute carbon monoxide poisoning. Brain Res, 2016. 1633: p. 62-72.
77. Hampson, N.B. and N.M. Hauff, Carboxyhemoglobin levels in carbon monoxide poisoning: do they correlate with the clinical picture? Am J Emerg Med, 2008. 26(6): p. 665-9.
78. Xiang, W., et al., P2Y12 receptor-mediated microglia activation involved in delayed encephalopathy after acute carbon monoxide poisoning. Aging (Albany NY), 2021. 13(4): p. 6134-6143.
79. National Research Council Committee on Acute Exposure Guideline, L., in Acute Exposure Guideline Levels for Selected Airborne Chemicals: Volume 8. 2010, National Academies Press (US) Copyright 2010 by the National Academy of Sciences. All rights reserved.: Washington (DC).
80. Murao, Y., et al., Effect of dose of hypertonic saline on its potential to prevent lung tissue damage in a mouse model of hemorrhagic shock. Shock, 2003. 20(1): p. 29-34.
81. Beaver, L.M., et al., Lung inflammation, injury, and proliferative response after repetitive particulate hexavalent chromium exposure. Environ Health Perspect, 2009. 117(12): p. 1896-902.
82. Gonzalez-Lopez, A., et al., Inflammation and matrix remodeling during repair of ventilator-induced lung injury. Am J Physiol Lung Cell Mol Physiol, 2011. 301(4): p. L500-9.
83. Kubiak, B.D., et al., Peritoneal negative pressure therapy prevents multiple organ injury in a chronic porcine sepsis and ischemia/reperfusion model. Shock, 2010. 34(5): p. 525-34.
84. Oami, T. and C.M. Coopersmith, Measurement of Intestinal Permeability During Sepsis. Methods Mol Biol, 2021. 2321: p. 169-175.
85. Watkins, D.J., et al., Synergistic effects of HB-EGF and mesenchymal stem cells in a murine model of intestinal ischemia/reperfusion injury. J Pediatr Surg, 2013. 48(6): p. 1323-9.
86. Wimon Phuntuwate1, S.R., Thawatchai Leelawittayanont1, Orawin Prangsaengtong1, Muthita Hirunsai1, Artitaya Boonrod1 and Somkiat Wattanasirichaigoon2, Protective Effect of N-acetylcysteine on Endotoxin-Induced Intestinal Permeability Dysfunction. Thai Pharm Health Sci J, 2006. 1(2): p. 19-25.
87. Bolger, A.M., M. Lohse, and B. Usadel, Trimmomatic: a flexible trimmer for Illumina sequence data. Bioinformatics, 2014. 30(15): p. 2114-20.
88. Edgar, R.C., et al., UCHIME improves sensitivity and speed of chimera detection. Bioinformatics, 2011. 27(16): p. 2194-200.
89. Haas, B.J., et al., Chimeric 16S rRNA sequence formation and detection in Sanger and 454-pyrosequenced PCR amplicons. Genome Res, 2011. 21(3): p. 494-504.
90. Lozupone, C. and R. Knight, UniFrac: a new phylogenetic method for comparing microbial communities. Appl Environ Microbiol, 2005. 71(12): p. 8228-35.
91. Lozupone, C., et al., UniFrac: an effective distance metric for microbial community comparison. ISME J, 2011. 5(2): p. 169-72.
92. Lozupone, C.A., et al., Quantitative and qualitative beta diversity measures lead to different insights into factors that structure microbial communities. Appl Environ Microbiol, 2007. 73(5): p. 1576-85.
93. Segata, N., et al., Metagenomic biomarker discovery and explanation. Genome Biol, 2011. 12(6): p. R60.
94. CLARKE, K.R., Non-parametric multivariate analyses of changes in community structure. Australian Journal of Ecology, 1993. 18(1): p. 117-143.
95. Arndt, D., et al., METAGENassist: a comprehensive web server for comparative metagenomics. Nucleic Acids Res, 2012. 40(Web Server issue): p. W88-95.
96. Asshauer, K.P., et al., Tax4Fun: predicting functional profiles from metagenomic 16S rRNA data. Bioinformatics, 2015. 31(17): p. 2882-4.
97. Wemheuer, F., et al., Tax4Fun2: prediction of habitat-specific functional profiles and functional redundancy based on 16S rRNA gene sequences. Environ Microbiome, 2020. 15(1): p. 11.
98. Arifin, W.N. and W.M. Zahiruddin, Sample Size Calculation in Animal Studies Using Resource Equation Approach. Malays J Med Sci, 2017. 24(5): p. 101-105.
99. Kotrlik, J.W. and H.A. Williams. The Incorporation of Effect Size in The Incorporation of Effect Size in Information Technology, Learning, Information Technology, Learning, and Performance Research and Performance Research. 2003.
100. Akoglu, H., User's guide to correlation coefficients. Turk J Emerg Med, 2018. 18(3): p. 91-93.
101. Holter, J.F., et al., Protein permeability in the adult respiratory distress syndrome. Loss of size selectivity of the alveolar epithelium. J Clin Invest, 1986. 78(6): p. 1513-22.
102. Wittekindt, O.H., Tight junctions in pulmonary epithelia during lung inflammation. Pflugers Arch, 2017. 469(1): p. 135-147.
103. Jang, J.H., et al., Acute respiratory distress syndrome caused by carbon monoxide poisoning and inhalation injury recovered after extracorporeal membrane oxygenation along with direct hemoperfusion with polymyxin B-immobilized fiber column: a case report. J Med Case Rep, 2021. 15(1): p. 456.
104. Liu, C., et al., Role of epithelial chemokines in the pathogenesis of airway inflammation in asthma (Review). Mol Med Rep, 2018. 17(5): p. 6935-6941.
105. Schutyser, E., et al., Regulated production and molecular diversity of human liver and activation-regulated chemokine/macrophage inflammatory protein-3 alpha from normal and transformed cells. J Immunol, 2000. 165(8): p. 4470-7.
106. Phaniendra, A., D.B. Jestadi, and L. Periyasamy, Free radicals: properties, sources, targets, and their implication in various diseases. Indian J Clin Biochem, 2015. 30(1): p. 11-26.
107. Evavold, C.L., et al., Control of gasdermin D oligomerization and pyroptosis by the Ragulator-Rag-mTORC1 pathway. Cell, 2021. 184(17): p. 4495-4511 e19.
108. Tang, D., et al., The molecular machinery of regulated cell death. Cell Res, 2019. 29(5): p. 347-364.
109. Youle, R.J. and A.M. van der Bliek, Mitochondrial fission, fusion, and stress. Science, 2012. 337(6098): p. 1062-5.
110. Canning, B.J. and J.L. Wright, Animal models of asthma and chronic obstructive pulmonary disease. Pulm Pharmacol Ther, 2008. 21(5): p. 695.
111. Tabrizian, K., et al., Magnesium sulfate protects the heart against carbon monoxide-induced cardiotoxicity in rats. Res Pharm Sci, 2018. 13(1): p. 65-72.
112. Thom, S.R., et al., Intravascular neutrophil activation due to carbon monoxide poisoning. Am J Respir Crit Care Med, 2006. 174(11): p. 1239-48.
113. Asgharian Rezaee, M., et al., Effects of erythropoietin on electrocardiogram changes in carbon monoxide poisoning: an experimental study in rats. Iran J Pharm Res, 2012. 11(4): p. 1191-9.
114. Xiang, W.P., H. Xue, and B.J. Wang, Delayed encephalopathy of acute carbon monoxide intoxication in rats: potential mechanism and intervention of dexamethasone. Pak J Pharm Sci, 2014. 27(6 Suppl): p. 2025-8.
115. Castro, A., et al., Impact of the wood combustion in an open fireplace on the air quality of a living room: Estimation of the respirable fraction. Sci Total Environ, 2018. 628-629: p. 169-176.
116. Wilbur S, W.M., Williams R, et al., Toxicological Profile for Carbon Monoxide. Atlanta (GA): Agency for Toxic Substances and Disease Registry (US). 2012 (POTENTIAL FOR HUMAN EXPOSURE.).
117. Yan, Y., et al., Exposure to hazardous air pollutants in underground car parks in Guangzhou, China. Air Quality, Atmosphere & Health, 2017. 10(5): p. 555-563.
118. Meyer, G., et al., Simulated urban carbon monoxide air pollution exacerbates rat heart ischemia-reperfusion injury. Am J Physiol Heart Circ Physiol, 2010. 298(5): p. H1445-53.
119. Reboul, C., et al., Carbon monoxide pollution aggravates ischemic heart failure through oxidative stress pathway. Sci Rep, 2017. 7: p. 39715.
120. Hohn, P., H. Gabbert, and R. Wagner, Differentiation and aging of the rat intestinal mucosa. II. Morphological, enzyme histochemical and disc electrophoretic aspects of the aging of the small intestinal mucosa. Mech Ageing Dev, 1978. 7(3): p. 217-26.
121. Keelan, M., K. Walker, and A.B. Thomson, Intestinal morphology, marker enzymes and lipid content of brush border membranes from rabbit jejunum and ileum: effect of aging. Mech Ageing Dev, 1985. 31(1): p. 49-68.
122. Martin, K., T.B. Kirkwood, and C.S. Potten, Age changes in stem cells of murine small intestinal crypts. Exp Cell Res, 1998. 241(2): p. 316-23.
123. Saffrey, M.J., Ageing of the enteric nervous system. Mech Ageing Dev, 2004. 125(12): p. 899-906.
124. Saffrey, M.J., Cellular changes in the enteric nervous system during ageing. Dev Biol, 2013. 382(1): p. 344-55.
125. Homma, H., et al., The female intestine is more resistant than the male intestine to gut injury and inflammation when subjected to conditions associated with shock states. Am J Physiol Gastrointest Liver Physiol, 2005. 288(3): p. G466-72.
126. O'donnell, D. and P. Laveneziana, Physiology and consequences of lung hyperinflation in COPD. European Respiratory Review, 2006. 15(100): p. 61-67.
127. Papandrinopoulou, D., V. Tzouda, and G. Tsoukalas, Lung compliance and chronic obstructive pulmonary disease. Pulm Med, 2012. 2012: p. 542769.
128. Moore, E., et al., Global Associations between Air Pollutants and Chronic Obstructive Pulmonary Disease Hospitalizations. A Systematic Review. Ann Am Thorac Soc, 2016. 13(10): p. 1814-1827.
129. Dong, L.L., et al., The persistent inflammation in COPD: is autoimmunity the core mechanism? Eur Respir Rev, 2024. 33(171).
130. Devos, F.C., et al., Forced expiration measurements in mouse models of obstructive and restrictive lung diseases. Respir Res, 2017. 18(1): p. 123.
131. Grace Umahi-Ottah, B.I.G.A., Elvis Osamede Godwins, Uchechukwu Dimkpa, Simon Uzor, Usman Itakure Abdulkadir, Oladimeji Nasiru Abdulrahman, Noreen Ebelechukwu Agbapuonwu, Onochie Anslem Ajugwo, Musiliu Adewale Oyenike, The Effects of Cigarette Smoking on Serum Carboxyhemoglobin and Calcium Levels in Apparently Healthy Male Smokers in Benin City, Nigeria. Journal of Biomedical Science and Engineering, 2022. 15(1).
132. Yang, I.A., C.R. Jenkins, and S.S. Salvi, Chronic obstructive pulmonary disease in never-smokers: risk factors, pathogenesis, and implications for prevention and treatment. Lancet Respir Med, 2022. 10(5): p. 497-511.
133. Kim, C.H., B. Park, and M.S. Baek, The effect of long-term exposure to a mixture of air pollutants on chronic obstructive pulmonary disease. Ecotoxicol Environ Saf, 2025. 292: p. 117978.
134. Hara, H., et al., Mitochondrial fragmentation in cigarette smoke-induced bronchial epithelial cell senescence. Am J Physiol Lung Cell Mol Physiol, 2013. 305(10): p. L737-46.
135. Kosmider, B., et al., Mitochondrial dysfunction in human primary alveolar type II cells in emphysema. EBioMedicine, 2019. 46: p. 305-316.
136. Liu, Q., et al., Attenuation of PM2.5-induced alveolar epithelial cells and lung injury through regulation of mitochondrial fission and fusion. Particle and Fibre Toxicology, 2023. 20(1): p. 28.
137. Zemirli, N., E. Morel, and D. Molino, Mitochondrial Dynamics in Basal and Stressful Conditions. Int J Mol Sci, 2018. 19(2).
138. Mizumura, K., et al., Mitophagy-dependent necroptosis contributes to the pathogenesis of COPD. J Clin Invest, 2014. 124(9): p. 3987-4003.
139. Zhang, Z., et al., Bcl-2 Proteins Regulate Mitophagy in Lipopolysaccharide-Induced Acute Lung Injury via PINK1/Parkin Signaling Pathway. Oxid Med Cell Longev, 2020. 2020: p. 6579696.
140. Thom, S.R., et al., Plasma biomarkers in carbon monoxide poisoning. Clin Toxicol (Phila), 2010. 48(1): p. 47-56.
141. Zhao, N., et al., After Treatment with Methylene Blue is Effective against Delayed Encephalopathy after Acute Carbon Monoxide Poisoning. Basic Clin Pharmacol Toxicol, 2018. 122(5): p. 470-480.
142. Di Stefano, A., et al., Association of increased CCL5 and CXCL7 chemokine expression with neutrophil activation in severe stable COPD. Thorax, 2009. 64(11): p. 968-75.
143. Ham, J., et al., The Dynamic Contribution of Neutrophils in the Chronic Respiratory Diseases. Allergy Asthma Immunol Res, 2022. 14(4): p. 361-378.
144. Dinarello, C.A., Overview of the IL-1 family in innate inflammation and acquired immunity. Immunol Rev, 2018. 281(1): p. 8-27.
145. Kotecha, S., et al., Increase in Interleukin (IL)-1β and IL-6 in Bronchoalveolar Lavage Fluid Obtained from Infants with Chronic Lung Disease of Prematurity. Pediatric Research, 1996. 40(2): p. 250-256.
146. Zenobia, C. and G. Hajishengallis, Basic biology and role of interleukin-17 in immunity and inflammation. Periodontol 2000, 2015. 69(1): p. 142-59.
147. Linden, A., M. Laan, and G.P. Anderson, Neutrophils, interleukin-17A and lung disease. Eur Respir J, 2005. 25(1): p. 159-72.
148. Moore, K.W., et al., Interleukin-10 and the interleukin-10 receptor. Annu Rev Immunol, 2001. 19: p. 683-765.
149. Kawano, H., et al., IL-10-producing lung interstitial macrophages prevent neutrophilic asthma. Int Immunol, 2016. 28(10): p. 489-501.
150. Soltys, J., et al., Functional IL-10 deficiency in the lung of cystic fibrosis (cftr(-/-)) and IL-10 knockout mice causes increased expression and function of B7 costimulatory molecules on alveolar macrophages. J Immunol, 2002. 168(4): p. 1903-10.
151. Hellenbrand, D.J., et al., Sustained interleukin-10 delivery reduces inflammation and improves motor function after spinal cord injury. J Neuroinflammation, 2019. 16(1): p. 93.
152. Bagheri, G., et al., Magnesium sulfate ameliorates carbon monoxide‑induced cerebral injury in male rats. Mol Med Rep, 2019. 19(2): p. 1032-1039.
153. Kinoshita, H., et al., Carbon monoxide poisoning. Toxicol Rep, 2020. 7: p. 169-173.
154. Nagpal, R. and H. Yadav, Bacterial Translocation from the Gut to the Distant Organs: An Overview. Ann Nutr Metab, 2017. 71 Suppl 1: p. 11-16.
155. Twardowska, A., et al., Preventing Bacterial Translocation in Patients with Leaky Gut Syndrome: Nutrition and Pharmacological Treatment Options. Int J Mol Sci, 2022. 23(6).
156. Rohm, T.V., et al., Inflammation in obesity, diabetes, and related disorders. Immunity, 2022. 55(1): p. 31-55.
157. Kojima, A., et al., Infection of specific strains of Streptococcus mutans, oral bacteria, confers a risk of ulcerative colitis. Sci Rep, 2012. 2: p. 332.
158. Wang, Y., et al., Ileal microbial microbiome and its secondary bile acids modulate susceptibility to nonalcoholic steatohepatitis in dairy goats. Microbiome, 2024. 12(1): p. 247.
159. Murros, K.E., et al., Desulfovibrio Bacteria Are Associated With Parkinson's Disease. Front Cell Infect Microbiol, 2021. 11: p. 652617.
160. Rowan, F., et al., Desulfovibrio bacterial species are increased in ulcerative colitis. Dis Colon Rectum, 2010. 53(11): p. 1530-6.
161. Zhang, X., et al., Dietary cholesterol drives fatty liver-associated liver cancer by modulating gut microbiota and metabolites. Gut, 2021. 70(4): p. 761-774.
162. Liang, B., et al., Fragile Guts Make Fragile Brains: Intestinal Epithelial Nrf2 Deficiency Exacerbates Neurotoxicity Induced by Polystyrene Nanoplastics. ACS Nano, 2024. 18(35): p. 24044-24059.
163. Kim, H.T., et al., Cholecystokinin attenuates β-cell apoptosis in both mouse and human islets. Translational Research, 2022. 243: p. 1-13.
164. Zhang, J.G., et al., Cholecystokinin octapeptide regulates the differentiation and effector cytokine production of CD4(+) T cells in vitro. Int Immunopharmacol, 2014. 20(2): p. 307-15.
165. De la Fuente, M., et al., Inhibition of murine peritoneal macrophage functions by sulfated cholecystokinin octapeptide. Regul Pept, 1995. 55(1): p. 47-56.
166. Carrasco, M., et al., Inhibition of human neutrophil functions by sulfated and nonsulfated cholecystokinin octapeptides. Peptides, 1997. 18(3): p. 415-22.
167. Fu, Y., et al., Gut Hormone GIP Induces Inflammation and Insulin Resistance in the Hypothalamus. Endocrinology, 2020. 161(9).
168. Chen, J., et al., GLP-1 receptor agonist as a modulator of innate immunity. Front Immunol, 2022. 13: p. 997578.
169. Leonov, G.E., et al., The Complicated Relationship of Short-Chain Fatty Acids and Oral Microbiome: A Narrative Review. Biomedicines, 2023. 11(10).
170. Zhou, H., et al., Effects of intestinal Desulfovibrio bacteria on host health and its potential regulatory strategies: A review. Microbiol Res, 2024. 284: p. 127725.
171. Frolova, M.S., et al., Genomic reconstruction of short-chain fatty acid production by the human gut microbiota. Front Mol Biosci, 2022. 9: p. 949563.
172. Brown, A.J., et al., The Orphan G protein-coupled receptors GPR41 and GPR43 are activated by propionate and other short chain carboxylic acids. J Biol Chem, 2003. 278(13): p. 11312-9.
173. Wan, Z., et al., FABP4-mediated lipid droplet formation in Streptococcus uberis-infected macrophages supports host defence. Vet Res, 2022. 53(1): p. 90.
174. Duan, R., et al., Flavonoids from Whole-Grain Oat Alleviated High-Fat Diet-Induced Hyperlipidemia via Regulating Bile Acid Metabolism and Gut Microbiota in Mice. J Agric Food Chem, 2021. 69(27): p. 7629-7640.
175. Qin, J., et al., A metagenome-wide association study of gut microbiota in type 2 diabetes. Nature, 2012. 490(7418): p. 55-60.
176. Yamamoto, T., et al., Mycoplasma pneumoniae drives macrophage lipid uptake via GlpD-mediated oxidation, facilitating foam cell formation. Int J Med Microbiol, 2025. 318: p. 151646.
177. Liu, J., et al., Gut microbiota and its metabolites regulate insulin resistance: traditional Chinese medicine insights for T2DM. Front Microbiol, 2025. 16: p. 1554189.
178. Koh, A., et al., Microbially Produced Imidazole Propionate Impairs Insulin Signaling through mTORC1. Cell, 2018. 175(4): p. 947-961.e17.
179. Du, L., et al., Gut microbiota-derived metabolites as key actors in type 2 diabetes mellitus. Biomed Pharmacother, 2022. 149: p. 112839.
180. Kong, L., et al., Trimethylamine N-oxide impairs β-cell function and glucose tolerance. Nat Commun, 2024. 15(1): p. 2526.
181. Shoelson, S.E., J. Lee, and A.B. Goldfine, Inflammation and insulin resistance. J Clin Invest, 2006. 116(7): p. 1793-801.
182. Ullah, H., et al., The gut microbiota-brain axis in neurological disorder. Front Neurosci, 2023. 17: p. 1225875.
183. Lyte, M., Microbial endocrinology and the microbiota-gut-brain axis. Adv Exp Med Biol, 2014. 817: p. 3-24.
184. Chen, Y., J. Xu, and Y. Chen, Regulation of Neurotransmitters by the Gut Microbiota and Effects on Cognition in Neurological Disorders. Nutrients, 2021. 13(6).
185. Bonnechère, B., N. Amin, and C. van Duijn, What Are the Key Gut Microbiota Involved in Neurological Diseases? A Systematic Review. Int J Mol Sci, 2022. 23(22).
186. Barnes-Velez, J.A., F.B. Aksoy Yasar, and J. Hu, Myelin lipid metabolism and its role in myelination and myelin maintenance. Innovation (Camb), 2023. 4(1): p. 100360.
187. Guo, D., H. Hu, and S. Pan, Oligodendrocyte dysfunction and regeneration failure: A novel hypothesis of delayed encephalopathy after carbon monoxide poisoning. Med Hypotheses, 2020. 136: p. 109522.
188. Yang, H., et al., Toxic effect of carbon monoxide and 41 inflammatory cytokines: A bidirectional 2-sample Mendelian randomization study. Medicine (Baltimore), 2025. 104(38): p. e44596.
189. Usuda, H., T. Okamoto, and K. Wada, Leaky Gut: Effect of Dietary Fiber and Fats on Microbiome and Intestinal Barrier. Int J Mol Sci, 2021. 22(14).
190. Al-Sadi, R., M. Boivin, and T. Ma, Mechanism of cytokine modulation of epithelial tight junction barrier. Front Biosci (Landmark Ed), 2009. 14(7): p. 2765-78.
191. Zhao, M., et al., Immunological mechanisms of inflammatory diseases caused by gut microbiota dysbiosis: A review. Biomed Pharmacother, 2023. 164: p. 114985.
192. Correa, R.O., et al., Butyrate: Connecting the gut-lung axis to the management of pulmonary disorders. Front Nutr, 2022. 9: p. 1011732.
193. Yang, J., et al., Lung-Gut Microbiota and Tryptophan Metabolites Changes in Neonatal Acute Respiratory Distress Syndrome. J Inflamm Res, 2024. 17: p. 3013-3029.
194. Cao, Y., et al., Farnesoid X receptor (FXR) as a potential therapeutic target for lung diseases: a narrative review. J Thorac Dis, 2024. 16(11): p. 8026-8038.
195. Hrenak, J. and F. Simko, Renin–Angiotensin System: An Important Player in the Pathogenesis of Acute Respiratory Distress Syndrome. International Journal of Molecular Sciences, 2020. 21(21): p. 8038.
196. Lang, C., et al., The role of the classical renin-angiotensin system and angiotensin-converting enzyme 2/Ang(1-7)/Mas axis in pulmonary fibrosis. Front Med (Lausanne), 2025. 12: p. 1615991.
197. Simoes e Silva, A.C., et al., ACE2, angiotensin-(1-7) and Mas receptor axis in inflammation and fibrosis. Br J Pharmacol, 2013. 169(3): p. 477-92.
198. Christofides, A., et al., The role of peroxisome proliferator-activated receptors (PPAR) in immune responses. Metabolism, 2021. 114: p. 154338.
199. Yoon, Y.S., et al., PPARγ activation following apoptotic cell instillation promotes resolution of lung inflammation and fibrosis via regulation of efferocytosis and proresolving cytokines. Mucosal Immunol, 2015. 8(5): p. 1031-46.
200. Necela, B.M. and E.A. Thompson, Pathophysiological Roles of PPARgamma in Gastrointestinal Epithelial Cells. PPAR Res, 2008. 2008: p. 148687.
201. Ji, J., et al., Potential Therapeutic Applications of Pulmonary Surfactant Lipids in the Host Defence Against Respiratory Viral Infections. Front Immunol, 2021. 12: p. 730022.
202. Bankaitis, V.A., The Cirque du Soleil of Golgi membrane dynamics. J Cell Biol, 2009. 186(2): p. 169-71.
203. Boldyreva, L.V., et al., Fat of the Gut: Epithelial Phospholipids in Inflammatory Bowel Diseases. Int J Mol Sci, 2021. 22(21).
204. Gomez-Larrauri, A., et al., The critical roles of bioactive sphingolipids in inflammation. J Biol Chem, 2025. 301(8): p. 110475.
205. Ueda, N., Ceramide-induced apoptosis in renal tubular cells: a role of mitochondria and sphingosine-1-phoshate. Int J Mol Sci, 2015. 16(3): p. 5076-124.
206. Petrache, I., et al., Ceramide upregulation causes pulmonary cell apoptosis and emphysema-like disease in mice. Nat Med, 2005. 11(5): p. 491-8.
207. Rohrhofer, J., et al., The Impact of Dietary Sphingolipids on Intestinal Microbiota and Gastrointestinal Immune Homeostasis. Front Immunol, 2021. 12: p. 635704.
208. Tsai, M.C., et al., High-altitude pulmonary edema can be prevented by heat shock protein 70-mediated hyperbaric oxygen preconditioning. J Trauma Acute Care Surg, 2014. 77(4): p. 585-91.
209. Bozok, S., et al., Protective effects of hyperbaric oxygen and iloprost on ischemia/reperfusion-induced lung injury in a rabbit model. Eur J Med Res, 2012. 17(1): p. 14.
210. Lu, M.Y., et al., Hyperbaric oxygen attenuates lipopolysaccharide-induced acute lung injury. Intensive Care Med, 2002. 28(5): p. 636-41.
211. Wu, N., et al., Myocardial and lung injuries induced by hydrogen sulfide and the effectiveness of oxygen therapy in rats. Clin Toxicol (Phila), 2011. 49(3): p. 161-6.
212. Hadanny, A., et al., Hyperbaric oxygen therapy effects on pulmonary functions: a prospective cohort study. BMC Pulm Med, 2019. 19(1): p. 148.
213. Sevda Comert, S.G.S., Benan Caglayan, Effects of a standard hyperbaric oxygen treatment protocol on pulmonary functions and diaphragm. European Respiratory Society, December 6, 2017. 50(61): p. 730.
214. Li, L., Clinical Nursing Experience Sharing of Patients with Severe Lung Injury Caused by Gas Poisoning. Appl Bionics Biomech, 2022. 2022: p. 4888524.
215. Weaver, L.K., Carbon monoxide poisoning. Undersea Hyperb Med, 2020. 47(1): p. 151-169.
216. Xu, D., T. Mei, and F. He, The neutrophil-to-lymphocyte ratio is associated with the frequency of delayed neurologic sequelae in patients with carbon monoxide poisoning. Sci Rep, 2023. 13(1): p. 19706.
217. Liao, S.C., et al., Real-world effectiveness of hyperbaric oxygen therapy for delayed neuropsychiatric sequelae after carbon monoxide poisoning. Sci Rep, 2021. 11(1): p. 19212.
218. Heyboer, M., 3rd, et al., Hyperbaric Oxygen Therapy: Side Effects Defined and Quantified. Adv Wound Care (New Rochelle), 2017. 6(6): p. 210-224.
219. Rose, J.J., et al., A neuroglobin-based high-affinity ligand trap reverses carbon monoxide-induced mitochondrial poisoning. J Biol Chem, 2020. 295(19): p. 6357-6371.
220. Lo Iacono, L., et al., A carbon monoxide-releasing molecule (CORM-3) uncouples mitochondrial respiration and modulates the production of reactive oxygen species. Free Radic Biol Med, 2011. 50(11): p. 1556-64.
221. Angelova, P.R., I. Myers, and A.Y. Abramov, Carbon monoxide neurotoxicity is triggered by oxidative stress induced by ROS production from three distinct cellular sources. Redox Biol, 2023. 60: p. 102598.
222. Zhang, R.G., C.Y. Yip, and W.H. Ko, Regulation of Intracellular Calcium by Carbon Monoxide in Human Bronchial Epithelial Cells. Cell Physiol Biochem, 2017. 42(6): p. 2377-2390.
223. Yu, H., et al., Impaired AT2 to AT1 cell transition in PM2.5-induced mouse model of chronic obstructive pulmonary disease. Respir Res, 2022. 23(1): p. 70.
224. Wang, Y., et al., Repair and regeneration of the alveolar epithelium in lung injury. FASEB J, 2024. 38(8): p. e23612.
225. Chow, W.K. and M.Y. Chan, Field measurement on transient carbon monoxide levels in vehicular tunnels. Building and Environment, 2003. 38(2): p. 227-236.
226. Gourdeau, P., M. Parent, and A. Soulard, Exposition à l'oxyde de carbone dans les garages d'automobiles: évaluation chez les mécaniciens. REVUE CANADIENNE DE SANTE PUBLIQUE: CANADIAN JOURNAL OF PUBLIC HEALTH, 1995. 86(6): p. 414-417.
227. Raub, J. and W.H. Organization, Carbon monoxide, in Carbon monoxide. 1999.
228. Shahryari, S., et al., Carbon Monoxide concentration, Visibility and Smoke Simulation Underground Railway Stations in Case of Emergency. 2014.
229. Winder, C., Carbon monoxide-induced death and toxicity from charcoal briquettes. Med J Aust, 2012. 197(6): p. 349-50.

簡易檢索 / 詳目顯示

相關論文