| Research Abstract |
IL-18 was recognized as a pro-inflammatory cytokine, which played important roles for induction of NO,ROI and TNF-α, via the production of IFN-γ with IL-12. Those factors were required for elimination of infectious microbes(Singh R.P., et al., J.Immunol.,2003), while those caused tissue damages(Shimmyo A.K., et al., J.Immunothera.,2002). However, in recent studies, we had revealed that IL-18 also carried the capability to induce anti-inflammatory cytokines, such as IL-4,IL-10 and IL-13 from T cells, NK cells and mast cells, in the absence of IL-12(Kashiwamura S., et al., J.Immunothera.,2002 ). In these studies, we had discussed new physiological roles of IL-18. When IL-18 was administered to mice with IL-12, this treatment caused liver steatosis by the impairment of micro circulation in the liver with induced excess NO(Kaneda M., et al., J.Interferon Cytokine Res.,2003). Further, it became clear that, the IL-18 concentration in the circulation highly related to the risk of myocardial infarction(Kawasaki D., et al., Am.J.Cardiol.,2003). High concentration of IL-18 was also observed in peritoneal fluid of the patients of endometriosis(Oku H., et al., Hum.Reprod.2004). In this study, we discovered that, IL-18 receptor was expressed in non-immune parenchymal cells in mucosal tissue, while IL-18 was expressed in infiltrating macrophages. Which implicated that, these parenchymal cells expressed COX-2 gene to produce PGE2 and suppressed inflammatory cytokines such as TNF-α, in response to IL-18.
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