肺炎支原体致炎的分子机制研究进展
发布时间：2019-03-06 21:35
【摘要】：肺炎支原体(Mycoplasma pneumoniae,Mp)是引起社区获得性肺炎的主要致病菌,以儿童多见,也可见于婴儿和老年患者。迄今为止Mp的致病性与致病机制尚不完全清楚。研究表明Mp感染后的炎症反应是支原体肺炎发生的主要机制,其致病机制主要包括3个方面:(1)Mp膜脂蛋白经机体TLR2识别后激活固有免疫系统,通过一系列信号转导途径诱导单核、巨噬细胞以及自然杀伤细胞等产生相应的促炎细胞因子和炎症介质;(2)Mp黏附至宿主细胞后可通过与TLR4相互作用诱导巨噬细胞自噬,最终诱导促炎细胞因子分泌;(3)Mp CARDS毒素可激活炎症小体,促进IL-1β分泌。因此,明确Mp的致病机制有助于现代治疗和预防性药物靶点的开发提供新的思路。
[Abstract]:Mycoplasma pneumoniae (Mycoplasma pneumoniae,Mp) is the main pathogen causing community-acquired pneumonia in children as well as in infants and elderly patients. So far, the pathogenicity and pathogenesis of Mp are not completely clear. The results show that the inflammatory reaction after Mp infection is the main mechanism of mycoplasma pneumonia, and its pathogenesis mainly includes three aspects: (1) Mp membrane lipoprotein activates the innate immune system after TLR2 recognition; Through a series of signal transduction pathways, monocytes, macrophages and natural killer cells were induced to produce corresponding pro-inflammatory cytokines and inflammatory mediators. (2) the adhesion of Mp to host cells can induce macrophage autophagy through interaction with TLR4, and finally induce the secretion of pro-inflammatory cytokines. (3) Mp CARDS toxin can activate inflammatory bodies and promote the secretion of IL-1 尾. Therefore, a clear understanding of the pathogenesis of Mp is helpful to modern treatment and the development of preventive drug targets to provide a new way of thinking.
【作者单位】： 南华大学医学院病原生物学研究所特殊病原体防控湖南省重点实验室湖南省分子靶标新药研究协同创新中心;
【基金】：国家自然科学基金(31670177)
【分类号】：R375.2
[Abstract]:Mycoplasma pneumoniae (Mycoplasma pneumoniae,Mp) is the main pathogen causing community-acquired pneumonia in children as well as in infants and elderly patients. So far, the pathogenicity and pathogenesis of Mp are not completely clear. The results show that the inflammatory reaction after Mp infection is the main mechanism of mycoplasma pneumonia, and its pathogenesis mainly includes three aspects: (1) Mp membrane lipoprotein activates the innate immune system after TLR2 recognition; Through a series of signal transduction pathways, monocytes, macrophages and natural killer cells were induced to produce corresponding pro-inflammatory cytokines and inflammatory mediators. (2) the adhesion of Mp to host cells can induce macrophage autophagy through interaction with TLR4, and finally induce the secretion of pro-inflammatory cytokines. (3) Mp CARDS toxin can activate inflammatory bodies and promote the secretion of IL-1 尾. Therefore, a clear understanding of the pathogenesis of Mp is helpful to modern treatment and the development of preventive drug targets to provide a new way of thinking.
【作者单位】： 南华大学医学院病原生物学研究所特殊病原体防控湖南省重点实验室湖南省分子靶标新药研究协同创新中心;
【基金】：国家自然科学基金(31670177)
【分类号】：R375.2
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