Insect fungal pathogens secrete a cell wall-associated glucanase that acts to help avoid recognition by the host immune system.

IF 6.7 1区 医学 Q1 Immunology and Microbiology
PLoS Pathogens Pub Date : 2023-08-09 eCollection Date: 2023-08-01 DOI:10.1371/journal.ppat.1011578
Huifang Wang, Zhuoyue Lu, Nemat O Keyhani, Juan Deng, Xin Zhao, Shuaishuai Huang, Zhibing Luo, Kai Jin, Yongjun Zhang
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引用次数: 1

Abstract

Fungal insect pathogens have evolved diverse mechanisms to evade host immune recognition and defense responses. However, identification of fungal factors involved in host immune evasion during cuticular penetration and subsequent hemocoel colonization remains limited. Here, we report that the entomopathogenic fungus Beauveria bassiana expresses an endo-β-1,3-glucanase (BbEng1) that functions in helping cells evade insect immune recognition/ responses. BbEng1 was specifically expressed during infection, in response to host cuticle and hemolymph, and in the presence of osmotic or oxidative stress. BbEng1 was localized to the fungal cell surface/ cell wall, where it acts to remodel the cell wall pathogen associated molecular patterns (PAMPs) that can trigger host defenses, thus facilitating fungal cell evasion of host immune defenses. BbEng1 was secreted where it could bind to fungal cells. Cell wall β-1,3-glucan levels were unchanged in ΔBbEng1 cells derived from in vitro growth media, but was elevated in hyphal bodies, whereas glucan levels were reduced in most cell types derived from the BbEng1 overexpressing strain (BbEng1OE). The BbEng1OE strain proliferated more rapidly in the host hemocoel and displayed higher virulence as compared to the wild type parent. Overexpression of their respective Eng1 homologs or of BbEng1 in the insect fungal pathogens, Metarhizium robertsii and M. acridum also resulted in increased virulence. Our data support a mechanism by which BbEng1 helps the fungal pathogen to evade host immune surveillance by decreasing cell wall glucan PAMPs, promoting successful fungal mycosis.

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昆虫真菌病原体分泌一种与细胞壁相关的葡聚糖酶,该酶有助于避免被宿主免疫系统识别。
真菌昆虫病原体进化出了多种逃避宿主免疫识别和防御反应的机制。然而,在表皮穿透和随后的血腔定植过程中,参与宿主免疫逃避的真菌因子的鉴定仍然有限。在这里,我们报道了昆虫病原真菌白僵菌表达一种内切-β-1,3-葡聚糖酶(BbEng1),其功能是帮助细胞逃避昆虫免疫识别/反应。BbEng1在感染期间、对宿主角质层和血淋巴的反应以及在渗透或氧化应激的存在下特异性表达。BbEng1定位于真菌细胞表面/细胞壁,在那里它可以重塑细胞壁病原体相关分子模式(PAMP),从而触发宿主防御,从而促进真菌细胞逃避宿主免疫防御。BbEng1是在可以与真菌细胞结合的地方分泌的。来自体外生长培养基的ΔBbEng1细胞的细胞壁β-1,3-葡聚糖水平没有变化,但在菌丝体中升高,而来自BbEng 1过表达菌株(BbEng1OE)的大多数细胞类型的葡聚糖水平降低。与野生型亲本相比,BbEng1OE菌株在宿主血腔中增殖更快,并表现出更高的毒力。它们各自的Eng1同源物或BbEng1在昆虫真菌病原体绿僵菌和吖啶菌中的过表达也导致毒力增加。我们的数据支持BbEng1通过减少细胞壁葡聚糖PAMP来帮助真菌病原体逃避宿主免疫监测的机制,从而促进真菌真菌病的成功。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
PLoS Pathogens
PLoS Pathogens 生物-病毒学
CiteScore
11.40
自引率
3.00%
发文量
598
审稿时长
2 months
期刊介绍: Bacteria, fungi, parasites, prions and viruses cause a plethora of diseases that have important medical, agricultural, and economic consequences. Moreover, the study of microbes continues to provide novel insights into such fundamental processes as the molecular basis of cellular and organismal function.
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