Kamaladevi Arumugam, Balamurugan Krishnaswamy
Department of Biotechnology, Alagappa University, Karaikudi 630 004, Tamil Nadu, India.
Department of Biotechnology, Alagappa University, Karaikudi 630 004, Tamil Nadu, India
Pathog Dis. 2015 Jul;73(5). doi: 10.1093/femspd/ftv021. Epub 2015 Mar 27.
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.
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。
