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논문 기본 정보

자료유형
학술저널
저자정보
Ik-Hwan Han (Hanyang University College of Medicine) Sung Young Goo (Yonsei University College of Medicine) Soon-Jung Park (Yonsei University College of Medicine) Se-Jin Hwang (Hanyang University College of Medicine) Yong-Seok Kim (Hanyang University College of Medicine) Michael Sungwoo Yang (Indianhead International School) Myoung-Hee Ahn (Hanyang University College of Medicine) Jae-Sook Ryu (Hanyang University College of Medicine)
저널정보
대한기생충학열대의학회 Parasites, Hosts and Diseases The Korean Journal of Parasitology Vol.47 No.3
발행연도
2009.9
수록면
205 - 212 (8page)

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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-αproduction 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-αproduction in macrophages through NO-dependent activation of NF-κB, which might be closely involved in inflammation caused by T. vaginalis.

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Abstract
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

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