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.
Citations
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