Gräb Jessica, Rybniker Jan
Department I of Internal Medicine, Division of Infectious Diseases, University of Cologne, Cologne, Germany.
Center for Molecular Medicine Cologne, University of Cologne, Cologne, Germany.
Microbiol Insights. 2019 Jul 24;12:1178636119864594. doi: 10.1177/1178636119864594. eCollection 2019.
The p38 mitogen-activated protein kinase (MAPK) is involved in a multitude of essential cellular processes. The kinase is activated in response to environmental stresses, including bacterial infections and inflammation, to regulate the immune response of the host. However, recent studies have demonstrated that pathogens can manipulate p38 MAPK signaling for their own benefit to either prevent or induce host cell apoptosis. In addition, there is evidence demonstrating that p38 MAPK is a potent trigger of pathogen-induced necrosis driven by mitochondrial membrane disruption. Given the large number of p38 MAPK inhibitors that have been tested in clinical trials, these findings provide an opportunity to repurpose these drugs for improved control of infectious diseases.
p38丝裂原活化蛋白激酶（MAPK）参与多种重要的细胞过程。该激酶在响应包括细菌感染和炎症在内的环境应激时被激活，以调节宿主的免疫反应。然而，最近的研究表明，病原体可以为自身利益操纵p38 MAPK信号传导，以预防或诱导宿主细胞凋亡。此外，有证据表明p38 MAPK是由线粒体膜破坏驱动的病原体诱导坏死的有效触发因素。鉴于大量p38 MAPK抑制剂已在临床试验中进行测试，这些发现为重新利用这些药物以更好地控制传染病提供了机会。
