陰道鞭毛蟲 (Trichomonas vaginalis) 是一種厭氧性的單細胞原生寄生蟲，感染所引起的陰道鞭毛蟲症 (trichomoniasis vaginalis) 是最常見的非病毒的性接觸傳染疾病。已知研究指出陰道鞭毛蟲的感染會引發感染部位的急性發炎傷害，伴隨著有許多陰道鞭毛蟲的存在、嗜中性白血球的浸潤以及上皮細胞的破壞。依據本實驗室先前的研究以及臨床的研究結果指出，嗜中性白血球的趨化激素 IL-8 可表現於陰道鞭毛蟲症患者之患處，以及與陰道鞭毛蟲共同培養的子宮頸上皮細胞上，但這些受到趨化作用而浸潤到感染處的嗜中性白血球是如何與陰道鞭毛蟲進行交互作用，這個部分仍不是非常清楚。在本篇研究中，利用嗜中性白血球的細胞株 HL-60 與陰道鞭毛蟲進行共同培養。我們發現越多的陰道鞭毛蟲存在，會造成 dHL-60 (differentiated HL-60) 產生內生性的活性氧分子 (reactive oxygen species, ROS) 越低，這是一個存在有感染程度以及時間性的調控關係。在 cytokine microarray 及 RT-PCR 的結果顯示，當陰道鞭毛蟲與 dHL-60 共同培養後，會引發細胞激素及趨化激素 IL-1β、TNF-α 及 IL-8 表現上升，ATP6AP1 則是有下降表現的現象。進一步，我們同樣利用 RT-PCR 的方式，觀察陰道鞭毛蟲的 oxygen scavenging system 的基因是否會與 dHL-60 共同培養後所產生的反應。我們發現在與 dHL-60共同培養的條件下，會造成不同程度 superoxide dismutase 6 (SOD6)、紅素氧還蛋白 rubrerythrin (RBR) 以及 thioredoxin peroxide (TrxP) 這些基因的表現。以上結果指出，陰道鞭毛蟲或許可以藉由降低宿主細胞活性氧分子的產生、調節細胞激素的表現，或者提升自身清除氧化物的能力來逃避先天性免疫反應的攻擊。

Trichomoniasis vaginalis, is one of the most common non-viral sexually transmitted diseases in human and caused by infection an anaerobic protist Trichomonas vaginalis. It is known that infection elicits a profuse, acute, inflammatory discharge containing many trichomonads, neutrophils infiltration and epithelial cells destruction. Although our and clinical studies showed chemoattractants of neutrophils, such as IL-8, are found in vitro culture between T. vaginalis and cervical epithelial cell or vaginal discharges of symptomatic trichomoniasis patients, not much concern about the interaction between infiltrated neutrophil and T. vaginalis. In this study, NBT assay and flow cytometric results show more T. vaginalis incubate with dHL-60 cells, that are neutrophil-like cell line, but less intracellular reactive oxygen species (ROS) generate from dHL-60 cells in a dose- and time-dependent manner. In the cytokine microarray and RT-PCR results, we find IL-1β and IL-8 and TNF-α of dHL-60 cells are up-regulated.and down-regulated ATP6AP1. Moreover, genes of trichomonad’s oxygen scavenge system such as superoxide dismutase 6 (SOD6), rubrerythrin (Rbr) and thioredoxin peroxidase (TrxP) are up-regulated while co-incubation with dHL-60. These results suggest that T. vaginalis may escape from innate immune response by decreasing ROS production, regulating pro-inflammatory cytokine expression and decreasing and increase self-oxygen detoxication mechanism.

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