空氣污染物PM10 (粒徑<10μm) 中的超細微粒(粒徑<100nm)的粒子被提出與慢性阻塞性肺病(COPD)致病過程有關。COPD 表徵之一肺氣腫，為肺泡壁受到破壞使得肺泡擴大，進而減弱肺泡彈性且降低肺部氣體交換功能。但是超細微粒如何導致肺部傷害機轉尚未有清楚的了解。因此本研究之目的要探討超細微碳黑是否造成肺泡壁的破壞與造成破壞之機轉。本研究將14nm之超細微碳黑(ufCB)以氣管插管方式注入C57BL/6公鼠肺部後(300μg/mouse)，分別在暴露後1、3、7與14天犧牲，收集其肺沖洗液與肺組織評估發炎反應與肺部組織破壞之程度。初步的結果顯示，暴露ufCB後，肺部的嗜中性白血球聚集增加，肺沖洗液中的蛋白質量與乳酸去氫(LDH)活性也有顯著性的上升，並且持續到14天。測量肺沖洗液中代表彈力蛋白的鎖鋉素(Desmosine)與代表膠原蛋白的指標羥脯氨酸(Hydroxyproline)的總量都在暴露後第1天顯著性上升並且持續到14天。此外，藉由組織染色發現，暴露超細微粒碳黑肺泡細胞之彈力蛋白呈現不連續且較細的現象。嗜中性白血球彈力(Neutrophils elastase)在暴露後第三天達最高量，而與金屬基質蛋白分解MMP-2與MMP-9的活性也顯著性的提高，以第一天的活性最大。而給予腹腔注射嗜中性白血球抗體後，可降低超細微粒誘發之嗜中性白血球彈力與金屬基質蛋白分解MMP-2與MMP-9的活性，並且減少肺沖洗液中之鎖鍊素與羥脯氨酸。
歸納以上的結果，暴露ufCB確實會使肺部之連結組織破壞。不但使肺泡細胞死亡並且引發肺部嗜中性白血球聚集增加，而細胞外基質結構受到破壞。這樣的影響與由嗜中性白血球所釋放出來的嗜中性白血球彈力和金屬基質蛋白分解-9的活性有相關性。

Ultrafine fraction (<100nm in diameter) of PM10 has been hypothesized in the development of chronic obstructive pulmonary disease (COPD), with the presence of airflow limitation due to chronic bronchitis, and emphysema (alveolar wall destruction). However, the mechanism is not well characterized. The objective of this study was to investigate whether ultrafine particles caused alveolar wall destruction and the mechanism contributing the destruction. We treated C57BL/6 male mice with a single intratracheal instillation of 300 µg ultrafine carbon black (ufCB; 14 nm in diameter) and collected lung tissue and bronchoalveolar lavage (BAL) fluid 24 hour, 3 days, 7 days and 14 days after exposure. The results indicated that ufCB treatment led to significantly sustained increases of neutrophils influx, total proteins and lactate dehydrogenase (LDH) activity in BAL fluid. Desmosine, indicator of elastin damage, and hydroxyproline, indicator for collagen damage, were significantly increased up to 14 day post-exposure to ufCB. Verhoeff-Van Gieson staining revealed weak and discontinuous pattern of elastic fiber along alveolar septa in ufCB-exposed mice. Neutrophils elastase activity was found to be significantly elevated, with the peak elevation at 3 days post-exposure. The activities of matrix metalloproteinase, MMP-2 and MMP-9, in BAL fluid were also significantly elevated, with the peak elevation at 1 day post-exposure. Most significantly, pretreatment with antibody against neutrophils reduced the number of neutrophils and activities of neutrophil elastase and MMP-9, preventing the increases of desmosine and hydroxyproline in BAL fluid. MMP-2 activity was also decreased, inhibiting the increase of hydroxyproline in BAL fluid. We concluded that ufCB exposure could acutely cause connective tissue breakdown. This effect mediated mostly by proteases from neutrophils, elastase and MMP-9.

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