| Summary: | 碩士 === 國立成功大學 === 微生物及免疫學研究所 === 98 === 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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