Melanization of a meristematic mutant of Fonsecaea monophora increase the pathogenesis in a BALB/c mice infection model. Medical Mycology

Melanization of a meristematic mutant of Fonsecaea monophora increase the pathogenesis in a BALB/c mice infection model. Medical Mycology
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Fonsecaea monophora 分生组织突变体的黑色化增加了 BALB/c 小鼠感染模型的发病机制。

DOI:
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发表时间:
2018
期刊:
影响因子:
2.9
通讯作者:
minmin jiang
minmin jiang
中科院分区:
医学3区
文献类型:
--
作者:
xiqing li;junmin zhang;minmin jiang

文献摘要

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黑色素在体内染母细胞霉菌病制剂中的作用仍不清楚。在这项研究中,我们通过使用白化突变体在BALB/c小鼠感染模型中解决了这个问题,白化突变体是由单胞菌的黑化分生组织突变体产生的。感染后10-25dpi和7-15dpi的甲胎株和白化株感染小鼠的临床表现最严重。两组在15dpi(急性感染期)时的组织病理学检查相似,但在30dpi(持续感染期)和45dpi(恢复期)时不同。在45dpi时,黑化菌株感染组与白化菌株感染组相比,可见硬化体。发现黑化品系感染组在15dpi时TH2细胞因子显著升高,而白化品系感染组在15dpi和30dpi时TH1和TH17细胞因子的表达水平增加。综上所述,目前的数据支持了我们的推测,即单细胞裂殖吸虫分生组织突变体的黑化可以增加体内的致病作用。在BALB/c小鼠体内,抑制TH1和TH17,加剧黑化单胞菌的TH2能力是逃避宿主免疫系统识别和持续的关键。
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 formelanized 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.