A TRP Channel Senses Lysosome Neutralization by Pathogens to Trigger Their Expulsion.
A TRP Channel Senses Lysosome Neutralization by Pathogens to Trigger Their Expulsion.
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DOI：
10.1016/j.cell.2015.05.009
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发表时间：
2015-06-04
期刊：
影响因子：
64.5
通讯作者：
Abraham SN
中科院分区：
文献类型：
--
作者：
Miao Y;Li G;Zhang X;Xu H;Abraham SN
脊椎动物细胞已经进化出复杂的细胞自主防御程序，以监测感染的亚细胞区室并引起对抗反应。这些程序被病原体相关模式分子和细胞内病原体改变细胞微环境的各种策略激活。在这里，我们表明，当尿致病性E。大肠杆菌（UPEC）感染膀胱上皮细胞（BEC）时，它们被自噬靶向，但由于它们能够中和溶酶体pH而避免降解。这种变化由粘脂TRP通道3（TRPML3）检测，该通道是定位于溶酶体的瞬时受体电位阳离子通道。TRPML3激活然后自发地启动溶酶体胞吐，导致外泌体包裹的细菌的排出。这些研究揭示了一个细胞默认系统的溶酶体稳态，已增选的自主防御计划，以清除寄生虫病原体。
Vertebrate cells have evolved elaborate cell-autonomous defense programs to monitor subcellular compartments for infection and to evoke counter-responses. These programs are activated by pathogen-associated pattern molecules and by various strategies intracellular pathogens employ to alter cellular microenvironments. Here, we show that when uropathogenic E. coli (UPEC) infect bladder epithelial cells (BECs), they are targeted by autophagy but avoid degradation because of their capacity to neutralize lysosomal pH. This change is detected by mucolipin TRP channel 3 (TRPML3), a transient receptor potential cation channel localized to lysosomes. TRPML3 activation then spontaneously initiates lysosome exocytosis, resulting in expulsion of exosome-encased bacteria. These studies reveal a cellular default system for lysosome homeostasis that has been co-opted by the autonomous defense program to clear recalcitrant pathogens.
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影响因子：
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