PDF(Pubmed)
Abstract：
Mycoplasmas, the smallest self-replicating prokaryotes without a cell wall, are the most prevalent and extensively studied species in humans. They significantly contribute to chronic respiratory tract illnesses and pneumonia, with children and adolescents being particularly vulnerable. Mycoplasma pneumoniae (M. pneumoniae) infections typically tend to be self-limiting and mild but can progress to severe or even life-threatening conditions in certain individuals. Extrapulmonary effects often occur without pneumonia, and both intrapulmonary and extrapulmonary complications operate through separate pathological mechanisms. The indirect immune-mediated damage of the immune system, vascular blockages brought on by vasculitis or thrombosis and direct harm from invasion or locally induced inflammatory cytokines are potential causes of extrapulmonary manifestations due to M. pneumoniae. Proteins associated with adhesion serve as the primary factor crucial for the pathogenicity of M. pneumoniae, relying on a specialized polarized terminal attachment organelle. The type and density of these host receptors significantly impact the adhesion and movement of M. pneumoniae, subsequently influencing the pathogenic mechanism and infection outcomes. Adjacent proteins are crucial for the proper assembly of the attachment organelle, with variations in the genetic domains of P1, P40 and P90 surfaces contributing to the variability of clinical symptoms and offering new avenues for developing vaccines against M. pneumoniae infections. M. pneumoniae causes oxidative stress within respiratory tract epithelial cells by adhering to host cells and releasing hydrogen peroxide and superoxide radicals. This oxidative stress enhances the vulnerability of host cells to harm induced by oxygen molecules. The lack of superoxide dismutase and catalase of bacteria allows it to hinder the catalase activity of the host cell, leading to the reduced breakdown of peroxides. Lung macrophages play a significant role in managing M. pneumoniae infection, identifying it via Toll-like receptor 2 and initiating the myeloid differentiation primary response gene 88-nuclear factor κΒ signaling cascade. However, the precise mechanisms enabling M. pneumoniae to evade intracellular host defenses remain unknown, necessitating further exploration of the pathways involved in intracellular survival. The present comprehensive review delves into the pathogenesis of M. pneumoniae infection within the pulmonary system and into extrapulmonary areas, outlining its impact.
摘要：
支原体,没有细胞壁的最小的自我复制原核生物，是人类中最普遍和被广泛研究的物种。它们显著导致慢性呼吸道疾病和肺炎，儿童和青少年特别脆弱。肺炎支原体（M.肺炎）感染通常倾向于自限性和轻度，但在某些个体中可能发展为严重甚至危及生命的疾病。肺外影响通常在没有肺炎的情况下发生，肺内和肺外并发症都是通过不同的病理机制进行的。免疫系统的间接免疫介导的损伤，由血管炎或血栓形成引起的血管阻塞以及由侵袭或局部诱导的炎性细胞因子引起的直接伤害是肺炎支原体肺外表现的潜在原因.与粘附相关的蛋白质是肺炎支原体致病性的主要因素，依靠专门的极化末端附着细胞器。这些宿主受体的类型和密度显著影响肺炎支原体的粘附和运动，随后影响致病机制和感染结果。相邻的蛋白质对于附着细胞器的正确组装至关重要，与P1，P40和P90表面的遗传结构域的变化有助于临床症状的变异性，并为开发针对肺炎支原体感染的疫苗提供了新的途径。肺炎支原体通过粘附于宿主细胞并释放过氧化氢和超氧化物自由基而在呼吸道上皮细胞内引起氧化应激。这种氧化应激增强了宿主细胞对氧分子诱导的伤害的脆弱性。细菌缺乏超氧化物歧化酶和过氧化氢酶使其阻碍宿主细胞的过氧化氢酶活性，导致过氧化物的分解减少。肺巨噬细胞在管理肺炎支原体感染中发挥重要作用，通过Toll样受体2鉴定它，并启动髓样分化初级反应基因88-核因子κΒ信号级联。然而,使肺炎支原体逃避细胞内宿主防御的确切机制仍然未知，需要进一步探索参与细胞内存活的途径。本综述探讨肺炎支原体感染在肺系统内和肺外区域的发病机制。概述其影响。
