Modulation of host signaling in the inflammatory response by enteropathogenic Escherichia coli virulence proteins

Modulation of host signaling in the inflammatory response by enteropathogenic Escherichia coli virulence proteins
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DOI:
10.1038/cmi.2016.52
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发表时间:
2016-10
影响因子:
24.1
通讯作者:
X. Zhuang;Zijuan Chen;Chenxi He;Lin Wang;Ruixue Zhou;Dapeng Yan;Baoxue Ge
X. Zhuang;Zijuan Chen;Chenxi He;Lin Wang;Ruixue Zhou;Dapeng Yan;Baoxue Ge
中科院分区:
医学1区
文献类型:
--
作者:
X. Zhuang;Zijuan Chen;Chenxi He;Lin Wang;Ruixue Zhou;Dapeng Yan;Baoxue Ge

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为了成功感染宿主细胞并逃避宿主免疫应答,肠细菌病原体如肠致病性大肠杆菌(EPEC)通常使用III型分泌系统(T3 SS)。最近的研究结果表明,各种效应物通过T3 SS注入宿主细胞,并对炎症信号通路产生抑制作用,从而破坏对这些病原体的免疫反应。在这里,我们回顾了最近的研究,旨在解决的几个重要的炎症信号通路的调节EPEC效应蛋白,如核因子-κB(NF-κB)和丝裂原活化蛋白激酶(MAPK)途径,提供了深入了解这一未知领域的未完成的工作,并有助于确定新的位置在炎症信号网络中的EPEC效应。
To successfully infect host cells and evade the host immune response, a type III secretion system (T3SS) is commonly used by enteric bacterial pathogens such as enteropathogenic Escherichia coli (EPEC). Recent findings have revealed that various effectors are injected into host cells through the T3SS and exert an inhibitory effect on inflammatory signaling pathways, subverting the immune responses to these pathogens. Here we review recent studies aimed at addressing the modulation of several important inflammatory signaling pathways modulated by EPEC effector proteins, such as the nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) pathways, which provides insight into the unfinished work in this unexplored field and helps to identify novel positions in inflammatory signaling networks for EPEC effectors.