沙门菌毒力岛引发持续性感染机制的研究进展

Role of pathogenicity islands in Salmonella during persistent infection

摘要:

沙门菌是一种重要的人兽共患食源性病原菌。其感染宿主后可以凭借独特的免疫逃逸机制逃避宿主免疫系统的清除，潜伏在宿主体内1年至终身不等，从而建立持续性感染。沙门菌持续性感染与毒力岛密切相关，尤其是沙门菌毒力岛（Salmonella pathogenicity islands，SPIs） SPI-1和SPI-2。SPI-1效应蛋白SipB和SipC等以不同的途径影响细菌入侵，诱导细胞自噬或者凋亡；而SPI-2效应蛋白SseI和SseL等可以通过调控不同的信号通路协助沙门菌的胞内存活，为沙门菌持续性感染的发生和发展提供条件。本文主要阐述SipB和SseI等毒力岛效应蛋白在沙门菌持续性感染过程中的作用，同时总结了SPI-6、SPI-7和SPI-19等毒力岛的作用，以期为研究沙门菌持续性感染提供新思路。

Abstract:

Salmonella are a major group of zoonotic foodborne pathogens. After infection, Salmonella can escape the clearance of host immune system by virtue of its unique immune escape mechanism and lurk in the host for over a year to establish persistent infection. The persistent infection of Salmonella is associated with the expression of Salmonella pathogenicity islands (SPIs), especially SPI-1 and SPI-2. SPI-1 effector proteins SipB and SipC affect bacterial invasion and induce autophagy or apoptosis in different ways. SPI-2 effector proteins SseI and SseL can assist the intracellular survival of Salmonella by regulating different signaling pathways, so as provide conditions for the persistent infection of Salmonella. This paper expounds the roles of different effector proteins such as SipB and SseL in the persistent infection of Salmonella and summarizes the effects of SPIs such as SPI-6, SPI-7, and SPI-19, hoping to provide new ideas for treating the persistent infection of Salmonella.