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。
Mycoplasma pneumonia, a major pathogen of community-acquired pneumonias in human,occasionally cause diseases in infants and geriatrics. The pathogenicity and pathogenic mechanism of Mycoplasma pneumonia are not clear so far. Studies have shown that the inflammatory response induced by Mycoplasma pneumonia is the main mechanism of the occurrence of mycoplasma pneumonia, and its pathogenesis mainly includes three aspects： 1） Mycoplasma pneumonia membrane lipoprotein recognized by TLR2 can activate the innate immune system through a series of signal transduction pathways, ultimately induces the production of various of proinflammatory cytokines and inflammatory mediators generated by monocytes, macrophages, and natural killer cells; 2） Mycoplasma pneumonia elicits macrophage autophagy via interaction with TLR4 after its adherence to host cells, and eventually leading to the secretion of proinflammatory cytokines; 3） CARDS toxin of Mycoplasma pneumonia can raise the inflammasome and promote the secretion of IL-1β. Hence, illumination of the pathogenic mechanism of Mycoplasma pneumonia is great helpful to the development of alternative therapeutic or preventive drug targets.
出处
《免疫学杂志》
CAS
CSCD
北大核心
2017年第7期639-644,共6页
Immunological Journal
基金
国家自然科学基金(31670177)
关键词
肺炎支原体
脂蛋白
细胞黏附
Mycoplasma pneumonia
Lipoprotein
Cytoadherence
