Involvement of mast cell by crosstalk with vaginal epithelial cell in inflammation caused by Trichomonas vaginalis

초록

Mast cells have been reported to be present predominantly in the vaginal smear of patients infected with T. vaginalis. Our previous study described that the mast cells activated with T. vaginalis showed increased production of histamine and TNF-α. The excretory-secretory products of T. vaginalis induced increased chemotactic activity of RPMC (rat peritoneal mast cells), and showed passive cutaneous anaphylaxis in mice. In trichomoniasis, vaginal epithelial cell (VEC) has been thought to plays roles as immune responsive cell and as adherence site for growth of Trichomonas vaginalis. The adherence of T. vaginalis to VEC is known to be cytotoxic to VEC, and immunological active materials produced by this host-parasite coincubation may be expected to affect on mast cell placed in lamina propria of vaginal mucosa. In this study, we investigated whether the conditioned medium prepared by coincubation of vaginal epithelial cell with T. vaginalis could stimulate mast cell. Trichomonads-conditioned medium (TCM) was prepared from culture supernatants from MS74 stimulated with live T. vaginalis for 6 h, compared with culture supernatants of MS74 cultured without trichomonads (CM). When human mast cell line (HMC-1) were incubated with TCM or CM or T. vaginalis for 1 h, respectively, β-hexosaminidase release induced by TCM or trichomonads showed significant increase compared with that of CM. Inflammatory cytokines such as IL-8, IL-6 and TNF-α were significantly increased in HMC stimulated with TCM than those with CM. In addition to, HMC showed increased migration to TCM containing IL-8 and MCP-1, examined by chemotaxis assay. Therefore, it is suggested that human mast cell might increase release of β-hexosaminidase, inflammatory cytokines such as IL-8, IL-6 & TNF-α on stimulation with TCM, and migrate to TCM. In conclusion, mast cell may be involved in inflammatory response caused by T. vaginalis via crosstalk response with human vaginal epithelium. Keywords: Trichomonas vaginalis, Mast cell, Inflammation, Vaginal epithelial cell