【摘要】：肺炎支原體(Mycoplasma pneumoniae,Mp)是引起社區(qū)獲得性肺炎的主要致病菌,以?xún)和嘁?jiàn),也可見(jiàn)于嬰兒和老年患者。迄今為止Mp的致病性與致病機(jī)制尚不完全清楚。研究表明Mp感染后的炎癥反應(yīng)是支原體肺炎發(fā)生的主要機(jī)制,其致病機(jī)制主要包括3個(gè)方面:(1)Mp膜脂蛋白經(jīng)機(jī)體TLR2識(shí)別后激活固有免疫系統(tǒng),通過(guò)一系列信號(hào)轉(zhuǎn)導(dǎo)途徑誘導(dǎo)單核、巨噬細(xì)胞以及自然殺傷細(xì)胞等產(chǎn)生相應(yīng)的促炎細(xì)胞因子和炎癥介質(zhì);(2)Mp黏附至宿主細(xì)胞后可通過(guò)與TLR4相互作用誘導(dǎo)巨噬細(xì)胞自噬,最終誘導(dǎo)促炎細(xì)胞因子分泌;(3)Mp CARDS毒素可激活炎癥小體,促進(jìn)IL-1β分泌。因此,明確Mp的致病機(jī)制有助于現(xiàn)代治療和預(yù)防性藥物靶點(diǎn)的開(kāi)發(fā)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.
【作者單位】： 南華大學(xué)醫(yī)學(xué)院病原生物學(xué)研究所特殊病原體防控湖南省重點(diǎn)實(shí)驗(yàn)室湖南省分子靶標(biāo)新藥研究協(xié)同創(chuàng)新中心;
【基金】：國(guó)家自然科學(xué)基金(31670177)
【分類(lèi)號(hào)】：R375.2

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