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人类致病支原体对免疫反应的颠覆

Subversion of the Immune Response by Human Pathogenic Mycoplasmas.

作者信息

Qin Lianmei, Chen Yiwen, You Xiaoxing

机构信息

Institute of Pathogenic Biology, Hengyang Medical College, Hunan Provincial Key Laboratory for Special Pathogens Prevention and Control, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang, China.

出版信息

Front Microbiol. 2019 Aug 21;10:1934. doi: 10.3389/fmicb.2019.01934. eCollection 2019.

DOI:10.3389/fmicb.2019.01934
PMID:31497004
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6712165/
Abstract

Mycoplasmas are a large group of prokaryotes which is believed to be originated from Gram-positive bacteria via degenerative evolution, and mainly capable of causing a wide range of human and animal infections. Although innate immunity and adaptive immunity play crucial roles in preventing mycoplasma infection, immune response that develops after infection fails to completely eliminate this bacterium under certain circumstances. Thus, it is reasonable to speculate that mycoplasmas employ some mechanisms to deal with coercion of host defense system. In this review, we will highlight and provide a comprehensive overview of immune evasion strategies that have emerged in mycoplasma infection, which can be divided into four aspects: (i) Molecular mimicry and antigenic variation on the surface of the bacteria to evade the immune surveillance; (ii) Overcoming the immune effector molecules assaults: Induction of detoxified enzymes to degradation of reactive oxygen species; Expression of nucleases to degrade the neutrophil extracellular traps to avoid killing by Neutrophil; Capture and cleavage of immunoglobulins to evade humoral immune response; (iii) Persistent survival: Invading into the host cell to escape the immune damage; Formation of a biofilm to establish a persistent infection; (iv) Modulation of the immune system to down-regulate the intensity of immune response. All of these features increase the probability of mycoplasma survival in the host and lead to a persistent, chronic infections. A profound understanding on the mycoplasma to subvert the immune system will help us to better understand why mycoplasma is so difficult to eradicate and ultimately provide new insights on the development of therapeutic regimens against this bacterium in future.

摘要

支原体是一大类原核生物,据信它们是通过退化进化从革兰氏阳性菌演化而来,主要能够引发广泛的人类和动物感染。尽管固有免疫和适应性免疫在预防支原体感染中发挥着关键作用,但在某些情况下,感染后产生的免疫反应无法完全清除这种细菌。因此,有理由推测支原体采用了一些机制来应对宿主防御系统的胁迫。在本综述中,我们将重点介绍并全面概述支原体感染中出现的免疫逃逸策略,这些策略可分为四个方面:(i)细菌表面的分子模拟和抗原变异以逃避免疫监视;(ii)克服免疫效应分子的攻击:诱导解毒酶降解活性氧;表达核酸酶降解中性粒细胞胞外陷阱以避免被中性粒细胞杀死;捕获和裂解免疫球蛋白以逃避体液免疫反应;(iii)持续存活:侵入宿主细胞以逃避免疫损伤;形成生物膜以建立持续感染;(iv)调节免疫系统以下调免疫反应强度。所有这些特性都增加了支原体在宿主体内存活的概率,并导致持续性、慢性感染。深入了解支原体颠覆免疫系统的机制将有助于我们更好地理解为什么支原体如此难以根除,并最终为未来开发针对这种细菌的治疗方案提供新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7cf/6712165/19eaa73f6612/fmicb-10-01934-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7cf/6712165/19eaa73f6612/fmicb-10-01934-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7cf/6712165/19eaa73f6612/fmicb-10-01934-g001.jpg

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Microb Pathog. 2019 Jan;126:92-100. doi: 10.1016/j.micpath.2018.10.035. Epub 2018 Oct 29.
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Mycoplasma genitalium adhesin P110 binds sialic-acid human receptors.生殖道支原体黏附素 P110 结合唾液酸类人受体。
Nat Commun. 2018 Oct 26;9(1):4471. doi: 10.1038/s41467-018-06963-y.
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The Role of Lipoproteins in Mycoplasma-Mediated Immunomodulation.
支气管哮喘合并支原体肺炎感染患儿治疗前后血清炎症标志物及免疫功能的变化及其临床意义
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Invertebrate Model Mirrors the Pathogenic Potential of within the Natural Host.无脊椎动物模型反映了自然宿主内的致病潜力。
Transbound Emerg Dis. 2024 Mar 22;2024:3009838. doi: 10.1155/2024/3009838. eCollection 2024.
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Molecular mimicry in the pathogenesis of autoimmune rheumatic diseases.自身免疫性风湿性疾病发病机制中的分子模拟
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Pathogens. 2024 Nov 15;13(11):1003. doi: 10.3390/pathogens13111003.
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PLoS Pathog. 2023 Nov 8;19(11):e1011761. doi: 10.1371/journal.ppat.1011761. eCollection 2023 Nov.
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