生物
突变体
发病机制
体内
免疫系统
拉伤
暗色丝孢菌病
表型
着色芽生菌病
微生物学
免疫学
基因
解剖
生物化学
生物技术
作者
Minmin Jiang,Wenying Cai,Junmin Zhang,Ting Xie,Liyan Xi,Xiqing Li,Jiufeng Sun
摘要
The role of melanin in agents of chromoblastomycosis in vivo still remains unclear. In this study, we addressed the question in a BALB/c mice infection model by using an albino mutant, which generated from a melanized meristematic mutant of F. monophora. The most severe clinical manifestations of infected mice were observed at 10-25 dpi (day post infection) and 7-15 dpi for melanized and albino strain, respectively. Histopathologic examination were similar in both groups at 15 dpi (acute infection phase), but not at 30 dpi (sustained infection phase) and 45 dpi (recovery phase). Sclerotic body could be revealed in melanized strain infection group compare with albino strain infection group at 45 dpi. We found significantly elevated of TH2 cytokines in melanized strain infected group at 15 dpi, while increased expression level of TH1 and TH17 cytokines in albino strain infection group at 15 and 30 dpi. In conclusion, the present data addressed our speculation that melanization of this meristematic mutant of F. monophora could increase the pathogenesis in vivo. The inhibition of TH1 and TH17, exacerbated TH2 ability of melanized F. monophora is the key to escape the host immune system at the initial recognition and persistence in BALB/c mice.
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