PKA/KIN-1 mediates innate immune responses to bacterial pathogens in Caenorhabditis elegans
PKA/KIN-1 mediates innate immune responses to bacterial pathogens in Caenorhabditis elegans
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PKA/KIN-1 介导秀丽隐杆线虫对细菌病原体的先天免疫反应
DOI：
10.1177/1753425917732822
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发表时间：
2017-09
期刊：
影响因子：
--
通讯作者：
Ke-Qin Zhang
中科院分区：
文献类型：
--
作者：
Xiao Y;Fang Liu;Pei-ji Zhao;Cheng-Gang Zou;Ke-Qin Zhang
秀丽隐杆线虫是一种遗传学上易处理的生物体，是研究宿主先天免疫的重要模式动物。虽然C.线虫与病原体接触后，可能作为免疫功能的场所，最近的研究表明，神经系统可以控制线虫的先天免疫。优雅的在本报告中，我们证明了神经元中的蛋白激酶A（PKA）/KIN-1有助于C.优美的基因芯片分析显示PKA/KIN-1调控非神经元组织中一组抗菌效应物的表达，这些抗菌效应物是对沙门氏菌的先天性免疫应答所必需的。肠此外，PKA/KIN-1在S.肠道感染我们的研究结果表明，溶酶体信号分子参与自噬通过控制自噬流量，而不是自噬体的形成。自噬是宿主防御S.在多细胞动物中的肠道感染中，溶酶体途径还充当PKA/KIN-1信号传导的下游效应物用于先天免疫。我们的数据表明PKA通路有助于C.线虫通过从神经系统向周围组织发出信号来保护宿主免受病原体的侵害。
The genetically tractable organism Caenorhabditis elegans is a powerful model animal for the study of host innate immunity. Although the intestine and the epidermis of C. elegans that is in contact with pathogens are likely to function as sites for the immune function, recent studies indicate that the nervous system could control innate immunity in C. elegans. In this report, we demonstrated that protein kinase A (PKA)/KIN-1 in the neurons contributes to resistance against Salmonella enterica infection in C. elegans. Microarray analysis revealed that PKA/KIN-1 regulates the expression of a set of antimicrobial effectors in the non-neuron tissues, which are required for innate immune responses to S. enterica. Furthermore, PKA/KIN-1 regulated the expression of lysosomal genes during S. enterica infection. Our results suggest that the lysosomal signaling molecules are involved in autophagy by controlling autophagic flux, rather than formation of autophagosomes. As autophagy is crucial for host defense against S. enterica infection in a metazoan, the lysosomal pathway also acts as a downstream effector of the PKA/KIN-1 signaling for innate immunity. Our data indicate that the PKA pathway contributes to innate immunity in C. elegans by signaling from the nervous system to periphery tissues to protect the host against pathogens.
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DOI：
10.1523/jneurosci.18-08-02871.1998
发表时间：
1998-04
期刊：
The Journal of Neuroscience
影响因子：
--
作者：
A. Berger;A. Hart;J. M. Kaplan
通讯作者：
A. Berger;A. Hart;J. M. Kaplan
影响因子：
64.5
作者：
Meisel JD;Panda O;Mahanti P;Schroeder FC;Kim DH
通讯作者：
Kim DH
影响因子：
32.4
作者：
Visvikis, Orane;Ihuegbu, Nnamdi;Labed, Sid A.;Luhachack, Lyly G.;Alves, Anna-Maria F.;Wollenberg, Amanda C.;Stuart, Lynda M.;Stormo, Gary D.;Irazoqui, Javier E.
通讯作者：
Irazoqui, Javier E.
影响因子：
56.9
作者：
Garsin, DA;Villanueva, JM;Ausubel, FM
通讯作者：
Ausubel, FM
影响因子：
16.2
作者：
Keming Zhou;Yongming Dong;Qian Ge;Dan Zhu;W. Zhou;Xian-guang Lin;T. Liang;Zhengxing Wu;Tao Xu
通讯作者：
Keming Zhou;Yongming Dong;Qian Ge;Dan Zhu;W. Zhou;Xian-guang Lin;T. Liang;Zhengxing Wu;Tao Xu