自噬
生物
吞噬体
细胞生物学
效应器
先天免疫系统
免疫系统
微生物学
ATG16L1
自噬体
吞噬作用
生物化学
免疫学
细胞凋亡
作者
Shahab Shahnazari,Anton Namolovan,Jeremy Mogridge,Peter K. Kim,John H. Brumell
出处
期刊:Autophagy
[Informa]
日期:2011-09-01
卷期号:7 (9): 957-965
被引量:47
标识
DOI:10.4161/auto.7.9.16435
摘要
Autophagy plays a significant role in innate and adaptive immune responses to microbial infection. Some pathogenic bacteria have developed strategies to evade killing by host autophagy. These include the use of 'camouflage' proteins to block targeting to the autophagy pathway and the use of pore-forming toxins to block autophagosome maturation. However, general inhibition of host autophagy by bacterial pathogens has not been observed to date. Here we demonstrate that bacterial cAMP-elevating toxins from B. anthracis and V. cholera can inhibit host anti-microbial autophagy, including autophagic targeting of S. Typhimurium and latex bead phagosomes. Autophagy inhibition required the cAMP effector protein kinase A. Formation of autophagosomes in response to rapamycin and the endogenous turnover of peroxisomes was also inhibited by cAMP-elevating toxins. These findings demonstrate that cAMP-elevating toxins, representing a large group of bacterial virulence factors, can inhibit host autophagy to suppress immune responses and modulate host cell physiology.
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