糖基转移酶 galE 的缺失会损害单核细胞增多性李斯特菌的 InlB 锚定和致病性。

IF 5.5 1区 农林科学 Q1 IMMUNOLOGY Virulence Pub Date : 2024-12-01 Epub Date: 2024-11-04 DOI:10.1080/21505594.2024.2422539
Xiaowei Fang, Mei Yuan, Minghao Zheng, Qian Guo, Yuting Yang, Yuying Yang, Xiongyan Liang, Jing Liu, Chun Fang
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引用次数: 0

摘要

单核细胞增生李斯特菌(L. monocytogenes)是一种食源性细胞内病原体,可导致人类和动物的严重疾病。InlB 是单核细胞增生李斯特菌的主要内蛋白,它锚定在细菌表面,介导其侵入各种宿主细胞。最近的研究表明,单核细胞增多症血清 4b 型菌株细胞壁聚合物壁茶酸 (WTA) 的半乳糖基化对 InlB 在细胞表面的锚定至关重要。WTA 的半乳糖基化是由几种糖基转移酶协调作用实现的,包括 GalU、GalE、GtcA、GttA 和 GttB。在这些糖基转移酶中,GttA 和 GttB 是 4b 血清型菌株所特有的,而 GalE、GalU 和 GtcA 在所有血清型中都是保守的。GalE 在 InlB 锚定和单核细胞增多性乳酸杆菌致病性中的作用仍不清楚。在本研究中,我们删除了单核细胞增多性乳酸杆菌菌株 ScottA 中参与半乳糖基化的 galE 基因。我们发现,galE 基因缺失会减少 InlB 的锚定,减弱细菌对 Caco-2 细胞(人结直肠腺癌细胞)和 MGC803 细胞(人胃癌细胞)的粘附和侵袭,增加 RAW264.7 细胞(小鼠单核巨噬细胞白血病细胞)的吞噬作用,但会减少增殖,并减少感染小鼠的细菌负荷、死亡率和组织损伤。总之,galE 基因缺失大大降低了 InlB 的锚定性,削弱了单核细胞增多性淋巴瘤的致病性。这一发现为单核细胞增多性淋巴瘤细胞壁修饰与致病性之间的相关性提供了新的见解。
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Deletion of glycosyltransferase galE impairs the InlB anchoring and pathogenicity of Listeria monocytogenes.

Listeria monocytogenes (L. monocytogenes) is a foodborne intracellular pathogen that causes serious disease in both humans and animals. InlB is the major internalin protein of L. monocytogenes, which anchors to the bacterial surface and mediates its invasion into various host cells. Recent studies have shown that galactosylation of the cell wall polymer wall teichoic acid (WTA) is essential for InlB anchoring on the cell surface of L. monocytogenes serotype 4b strains. Galactosylation of WTA is exerted by the coordinated action of several glycosyltransferases, including GalU, GalE, GtcA, GttA, and GttB. Among these glycosyltransferases, GttA and GttB are specific to serotype 4b strains, whereas GalE, GalU, and GtcA are conserved across all serotypes. The role of GalE in InlB anchoring and L. monocytogenes pathogenicity remains unclear. In this study, we deleted the galE gene, which is involved in galactosylation, from L. monocytogenes strain ScottA. We found that galE deletion reduced InlB anchoring, weakened bacterial adhesion and invasion of Caco-2 cells (human colorectal adenocarcinoma cells) and MGC803 cells (human gastric carcinoma cells), increased phagocytosis but decreased proliferation in RAW264.7 cells (mouse mononuclear macrophage leukaemia cells), and decreased bacteria load, mortality, and tissue damage in infected mice. Taken together, galE deletion significantly reduced the anchoring of InlB and weakened the pathogenicity of L. monocytogenes. This finding provides new insights into the correlation between cell wall modification and pathogenicity of L. monocytogenes.

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来源期刊
Virulence
Virulence IMMUNOLOGY-MICROBIOLOGY
CiteScore
9.20
自引率
1.90%
发文量
123
审稿时长
6-12 weeks
期刊介绍: Virulence is a fully open access peer-reviewed journal. All articles will (if accepted) be available for anyone to read anywhere, at any time immediately on publication. Virulence is the first international peer-reviewed journal of its kind to focus exclusively on microbial pathogenicity, the infection process and host-pathogen interactions. To address the new infectious challenges, emerging infectious agents and antimicrobial resistance, there is a clear need for interdisciplinary research.
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