| Title | NF-κB/ROS and ERK pathways regulate NLRP3 inflammasome activation in Listeria monocytogenes infected BV2 microglia cells |
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| Author | Lin Yuan1,2, Yurong Zhu1,3, Shuang Huang1, Lin Lin1, Xugan Jiang1, and Shengxia Chen1* |
| Address | 1School of Medicine, Jiangsu University, Zhenjiang 212013, P. R. China, 2Department of Clinical Laboratory, Northern Jiangsu People' s Hospital, Yangzhou 225001, P. R. China, 3Department of Microbiology Laboratory, Linfen Central Hospital, Linfen 041000, P. R. China |
| Bibliography | Journal of Microbiology, 59(8),771–781, 2021, |
| DOI | 10.1007/s12275-021-0692-9 |
| Key Words | Listeria monocytogenes, nucleotide binding and oligomerization, leucine-rich repeat, pyrin domain-containing 3 (NLRP3) inflammasome, pyroptosis, microglia, nuclear factor kappa-B (NF-κB), reactive oxygen species (ROS), mitogen- activated protein kinase (MAPK) |
| Abstract | Listeria monocytogenes is a food-borne pathogen responsible for neurolisteriosis, which is potentially lethal in immunocompromised individuals. Microglia are the main target cells for L. monocytogenes in central nervous system (CNS). However, the precise mechanisms by which they trigger neuroinflammatory processes remain unknown. The BV2 microglial cell line and a murine model of L. monocytogenes infection were used for experiments in this study. Listeria monocytogenes induced pyroptosis and nucleotide binding and oligomerization, leucine-rich repeat, pyrin domain-containing 3 (NLRP3) inflammasome activation in BV2. Pharmacological inhibition of the NLRP3 inflammasome attenuated L. monocytogenes- induced pyroptosis. Moreover, inhibition of nuclear factor kappa-B (NF-κB) and extracellular regulated protein kinases (ERK) pathways induced a decrease in caspase1 activation and mature IL-1β-17 secretion. Our collective findings support critical involvement of the NLRP3 inflammasome in L. monocytogenes-induced neuroinflammation and, to an extent, ROS production. In addition, ERK and NF-κB signaling play an important role in activation of the NLRP3 inflammasome, both in vitro and in vivo. |