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Proinflammatory Cytokine and Nitric Oxide Production by Human Macrophages Stimulated with Trichomonas vaginalis

Korean Journal of Parasitology 2009년 47권 3호 p.205 ~ 212
 ( Han Ik-Hwan ) - 한양대학교 의과대학 기생충학교실

 ( Yang Sung-Woo Michael ) - Indianhead International School
김용석 ( Kim Yong-Seok ) - 한양대학교 의과대학 생화학교실
황세진 ( Hwang Se-Jin ) - 한양대학교 의과대학 해부.세포생물학교실
 ( Park Soon-Jung ) - 연세대학교 의과대학 환경의생물학교실
 ( Goo Sung-Young ) - 연세대학교 의과대학 환경의생물학교실
안명희 ( Ahn Myoung-Hee ) - 한양대학교 의과대학 기생충학교실
류재숙 ( Ryu Jae-Sook ) - 한양대학교 의과대학 기생충학교실

Abstract


Trichomonas vaginalis commonly causes vaginitis and perhaps cervicitis in women and urethritis in men and women. Macrophages are important immune cells in response to T. vaginalis infection. In this study, we investigated whether human macrophages could be involved in inflammation induced by T. vaginalis. Human monocyte-derived macrophages (HMDM) were co-cultured with T. vaginalis. Live, opsonized-live trichomonads, and T. vaginalis lysates increased proinflammatory cytokines, such as TNF-α, IL-1β, and IL-6 by HMDM. The involvement of nuclear factor (NF)-κB signaling pathway in cytokine production induced by T. vaginalis was confirmed by phosphorylation and nuclear translocation of p65 NF-κB. In addition, stimulation with live T. vaginalis induced marked augmentation of nitric oxide (NO) production and expression of inducible NO synthase (iNOS) levels in HMDM. However, trichomonad-induced NF-κB activation and TNF-α production in macrophages were significantly inhibited by inhibition of iNOS levels with L-NMMA (NO synthase inhibitor). Moreover, pretreatment with NF-κB inhibitors (PDTC or Bay11-7082) caused human macrophages to produce less TNF-α. These results suggest that T. vaginalis stimulates human macrophages to produce proinflammatory cytokines, such as IL-1, IL-6, and TNF-α, and NO. In particular, we showed that T. vaginalis induced TNF-α production in macrophages through NO-dependent activation of NF-κB, which might be closely involved in inflammation caused by T. vaginalis.

키워드

Trichomonas vaginalis;human monocyte-derived macrophage;proinflammatory cytokine;nitric oxide;iNOS;NF-κB
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