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题名: A Chitin-Like Component on Sclerotic Cells of Fonsecaea pedrosoi Inhibits Dectin-1-Mediated Murine Th17 Development by Masking beta-Glucans
作者: Dong, Bilin1; Li, Dongsheng1; Li, Ruoyu2; Chen, Sharon C. -A.3; Liu, Weihuang4; Liu, Wei5; Chen, Liuqing1; Chen, Yao1; Zhang, Xu1; Tong, Zhongsheng1; Xia, Yun1; Xia, Ping1; Wang, Yan5; Duan, Yiqun1
刊名: PLOS ONE
发表日期: 2014-12-09
DOI: 10.1371/journal.pone.0114113
卷: 9, 期:12
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Multidisciplinary Sciences
研究领域[WOS]: Science & Technology - Other Topics
英文摘要: Fonsecaea pedrosoi (F. pedrosoi), a major agent of chromoblastomycosis, has been shown to be recognized primarily by C-type lectin receptors (CLRs) in a murine model of chromoblastomycosis. Specifically, the beta-glucan receptor, Dectin-1, mediates Th17 development and consequent recruitment of neutrophils, and is evidenced to have the capacity to bind to saprophytic hyphae of F. pedrosoi in vitro. However, when embedded in tissue, most etiological agents of chromoblastomycosis including F. pedrosoi will transform into the sclerotic cells, which are linked to the greatest survival of melanized fungi in tissue. In this study, using immunocompetent and athymic (nu/nu) murine models infected subcutaneously or intraperitoneally with F. pedrosoi, we demonstrated that T lymphocytes play an active role in the resolution of localized footpad infection, and there existed a significantly decreased expression of Th17-defining transcription factor Ror gamma t and inefficient recruitment of neutrophils in chronically infected spleen where the inoculated mycelium of F. pedrosoi transformed into the sclerotic cells. We also found that Dectin-1-expressing histocytes and neutrophils participated in the enclosure of transformed sclerotic cells in the infectious foci. Furthermore, we induced the formation of sclerotic cells in vitro, and evidenced a significantly decreased binding capacity of human or murine-derived Dectin-1 to the induced sclerotic cells in comparison with the saprophytic mycelial forms. Our analysis of beta-glucans-masking components revealed that it is a chitin-like component, but not the mannose moiety on the sclerotic cells, that interferes with the binding of beta-glucans by human or murine Dectin-1. Notably, we demonstrated that although Dectin-1 contributed to the development of IL-17A-producing CD3+CD4+ murine splenocytes upon in vitro-stimulation by saprophytic F. pedrosoi, the masking effect of chitin components partly inhibited Dectin-1-mediated Th17 development upon in vitro-stimulation by induced sclerotic cells. Therefore, these findings extend our understanding of the chronicity of chromoblastomycosis.
关键词[WOS]: HOST-DEFENSE ; CHROMOBLASTOMYCOSIS ; RECEPTOR ; INFECTION ; IMMUNITY ; FORMS ; RECOGNITION ; CYTOKINES ; AGENT ; FUNGI
语种: 英语
WOS记录号: WOS:000347515300017
ISSN号: 1932-6203
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内容类型: 期刊论文
URI标识: http://ir.ihb.ac.cn/handle/342005/27132
Appears in Collections:分析测试中心_期刊论文

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作者单位: 1.1 Hosp Wuhan, Ctr Infect Skin Dis, Dept Dermatol, Wuhan, Peoples R China
2.Peking Univ, Res Ctr Med Mycol, Beijing 100871, Peoples R China
3.Univ Sydney, Westmead Hosp, ICPMR Pathol W, Ctr Infect Dis & Microbiol,Lab Serv, Westmead, NSW 2145, Australia
4.Wuhan Univ, Med Res Ctr, Wuhan 430072, Peoples R China
5.Chinese Acad Sci, Inst Hydrobiol, Wuhan, Peoples R China
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