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PMK-1/p38丝裂原活化蛋白激酶防御在秀丽隐杆线虫宿主-病原体相互作用期间抵抗肺炎克雷伯菌感染中的作用

Role of PMK-1/p38 MAPK defense in Caenorhabditis elegans against Klebsiella pneumoniae infection during host-pathogen interaction.

作者信息

Kamaladevi Arumugam, Balamurugan Krishnaswamy

机构信息

Department of Biotechnology, Alagappa University, Karaikudi 630 004, Tamil Nadu, India.

Department of Biotechnology, Alagappa University, Karaikudi 630 004, Tamil Nadu, India

出版信息

Pathog Dis. 2015 Jul;73(5). doi: 10.1093/femspd/ftv021. Epub 2015 Mar 27.

Abstract

The present study reports that Klebsiella pneumoniae (KP) killed the Caenorhabditis elegans as a consequence of an accumulation and proliferation of the pathogen inside the worms' intestine. The real-time PCR analysis of the genes responsible for vulval development (let-23) and egg laying (lin-29) in KP infected C. elegans confirmed the reproductive defects provoked by KP at the molecular level. In addition, the genetic analysis in N2 wild type, tol-1, sek-1 and pmk-1 mutants unveiled that KP attenuates the toll-dependent p38 mitogen-activated protein kinase (p38 MAPK) by chiefly inhibiting the production of antimicrobial factors such as nlp-29, lys-1 and C-type lectins. Conclusively, the surrendering of the host immune system appears to be attenuated by the toll-dependent p38 MAPK pathway regulation in C. elegans.

摘要

本研究报告称,肺炎克雷伯菌(KP)会导致秀丽隐杆线虫死亡,这是由于该病原体在蠕虫肠道内积累和增殖所致。对感染KP的秀丽隐杆线虫中负责外阴发育(let-23)和产卵(lin-29)的基因进行实时PCR分析,证实了KP在分子水平上引发的生殖缺陷。此外,对N2野生型、tol-1、sek-1和pmk-1突变体的遗传分析表明,KP主要通过抑制抗菌因子如nlp-29、lys-1和C型凝集素的产生,来减弱依赖Toll的p38丝裂原活化蛋白激酶(p38 MAPK)。总之,在秀丽隐杆线虫中,依赖Toll的p38 MAPK途径调节似乎会减弱宿主免疫系统的反应。

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