Miura Noriko N, Komai Motohiko, Adachi Yoshiyuki, Osada Naoki, Kameoka Yosuke, Suzuki Kazuo, Ohno Naohito
Laboratory for Immunopharmacology of Microbial Products, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
J Immunol. 2009 Sep 1;183(5):3417-24. doi: 10.4049/jimmunol.0802484. Epub 2009 Aug 12.
Candida albicans water-soluble fraction (CAWS), a mannoprotein-beta-glucan complex obtained from the culture supernatant of C. albicans NBRC1385, exhibits vasculitis-inducing activity (CAWS-vasculitis) in mice. The sensitivity to CAWS-vasculitis varies greatly among mouse strains. This study examined the factors contributing to or inhibiting CAWS-vasculitis using CAWS-vasculitis-resistant CBA/J mice and Bruton's tyrosine kinase-deficient CBA/N mice, which is a CAWS-vasculitis-sensitive strain that has the same origin as CBA/J mice. After stimulation with various kinds of pathogen-associated molecular patterns, the production of inflammatory cytokines IL-6 and IFN-gamma was induced in CBA/N mice, whereas that of immunosuppressive IL-10 was induced in CAWS-vasculitis-resistant CBA/J mice. Furthermore, the production of tissue inhibitor of metalloproteinase 1, an endogenous matrix metalloproteinase inhibitor, was observed in CBA/J mice. The results strongly suggest that the difference in the production of these cytokines is closely linked to the development of CAWS-vasculitis.
白色念珠菌水溶性组分（CAWS）是一种从白色念珠菌NBRC1385培养上清液中获得的甘露糖蛋白 - β - 葡聚糖复合物，在小鼠中表现出诱导血管炎的活性（CAWS - 血管炎）。小鼠品系对CAWS - 血管炎的敏感性差异很大。本研究使用对CAWS - 血管炎具有抗性的CBA/J小鼠和布鲁顿酪氨酸激酶缺陷的CBA/N小鼠（这是一种与CBA/J小鼠起源相同的对CAWS - 血管炎敏感的品系），研究了促成或抑制CAWS - 血管炎的因素。在用各种病原体相关分子模式刺激后，CBA/N小鼠中诱导了炎性细胞因子IL - 6和IFN - γ的产生，而在对CAWS - 血管炎具有抗性的CBA/J小鼠中诱导了免疫抑制性IL - 10的产生。此外，在CBA/J小鼠中观察到了金属蛋白酶组织抑制剂1（一种内源性基质金属蛋白酶抑制剂）的产生。结果强烈表明，这些细胞因子产生的差异与CAWS - 血管炎的发展密切相关。
