肺炎链球菌与宿主炎症小体的相互作用机制

肺炎链球菌(Streptococcus pneumoniae)是一种定植于上呼吸道的革兰阳性胞外菌,是导致侵袭性肺炎的主要原因,所致疾病具有较高的发病率和死亡率。炎症小体(inflammasome)是胞浆内重要的蛋白复合体,在先天免疫应答过程中起着重要作用。大量研究表明,肺炎链球菌感染可诱导宿主炎症小体的激活、半胱天冬酶1的活化和促炎性细胞因子的分泌。在长期选择压力的作用下,肺炎链球菌的部分突变菌株可以逃避炎症小体的识别。本文就肺炎链球菌感染过程中炎症小体的激活、炎症小体在抗肺炎链球菌过程中的作用以及肺炎链球菌逃避宿主炎症小体识别的机制三方面对肺炎链球菌与炎症小体之间相互作用的研究进展进行综述。

Mechanisms underlying the interaction between Streptococcus pneumoniae and host inflammasomes

Streptococcus pneumoniae is a Gram-positive extracellular bacterium colonized in the upper respiratory tract, and the main cause of invasive pneumonia with high morbidity and mortality. Inflammasomes are multi-protein complexes located in the cytosol and critical in innate immune responses. Numerous studies have shown that S. pneumoniae infection can induce the assembling of inflammasomes, activation of caspase-1 and secretion of pro-inflammatory cytokines. Under the long-term selection pressure, S. pneumoniae evolves with some mutations to escape inflammasome recognition. In this review, mechanisms on the interactions between S. pneumoniae and host inflammasomes, including the induction and active role of inflammasomes during S. pneumoniae infection, and the evasion strategy of S. pneumoniae against inflammasome recognition are summarized.