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Toll-like receptor 2 signaling pathway activation contributes to a highly efficient inflammatory response in Japanese

Guanyu Zhao1, Yan Gao2, Jiaqi Zhang2

  • 1College of Veterinary Medicine, College of Animal Science, Jilin University, Changchun, China.

Frontiers in Microbiology
|September 29, 2022
PubMed

Insights

Japanese encephalitis virus (JEV) triggers an inflammatory response in microglia via toll-like receptor 2 (TLR2). This study reveals the TLR2-PI3K-AKT pathway is critical in early JEV infection stages.

Area of Science:

  • Neuroimmunology
  • Virology
  • Cellular Biology

Background:

  • Japanese encephalitis (JE) is a severe disease caused by the Japanese encephalitis virus (JEV), often exacerbated by an overactive inflammatory response.
  • Microglia, the central nervous system's immune cells, are crucial in combating JEV infections.
  • The specific role of toll-like receptor 2 (TLR2) in the early inflammatory response to JEV in microglia remains unclear.

Purpose of the Study:

  • To investigate the protein expression profiles of JEV-infected BV2 microglia cells.
  • To elucidate the involvement of TLR2 in the early inflammatory response during JEV infection.
  • To identify key signaling pathways mediating the inflammatory response to JEV.

Main Methods:

  • Quantitative proteomics using tandem mass tags (TMT) labeling to analyze protein expression at 6, 12, and 24 hours post-infection (hpi).
  • Bioinformatic analysis (Gene Ontology and KEGG pathway enrichment) to identify biological functions of differentially expressed proteins.
  • Validation using parallel reaction monitoring (PRM), western blotting, and quantitative PCR (qPCR).
  • Inhibition assays targeting TLR2, PI3K, and AKT to determine pathway involvement.

Main Results:

  • Proteomic analysis identified significant upregulation of immune response-related proteins at 6, 12, and 24 hpi (212, 754, and 191 proteins, respectively).
  • The MyD88-dependent pathway (IRAK1, IRAK4, TRAF6) was not activated; however, the PI3K-AKT pathway showed increased expression.
  • Inhibition of TLR2, PI3K, or AKT confirmed JEV-induced activation of TLR2 and a subsequent inflammatory response.
  • The TLR2-PI3K-AKT signaling axis was identified as critical in the early inflammatory response to JEV.

Conclusions:

  • JEV infection activates microglia through the TLR2 signaling pathway.
  • The TLR2-PI3K-AKT axis plays a crucial role in mediating the early inflammatory response during JEV infection in microglia.
  • Targeting the TLR2-PI3K-AKT pathway may offer therapeutic strategies for Japanese encephalitis.
Keywords:
Japanese encephalitis virus (JEV)inflammatory responsemicroglialproteomicstoll-like receptor 2 (TLR2)

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