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In Vitro Analysis of Myd88-mediated Cellular Immune Response to West Nile Virus Mutant Strain Infection
Published on: November 27, 2014
IL-22 signaling contributes to West Nile encephalitis pathogenesis
Penghua Wang1, Fengwei Bai, Lauren A Zenewicz
1Section of Infectious Diseases, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, USA. penghua.wang@yale.edu
Plos One
|September 7, 2012
Summary
Interleukin-22 (IL-22) signaling worsens West Nile virus (WNV) encephalitis. Mice lacking IL-22 showed reduced neuroinflammation and were more resistant to lethal WNV infection.
Area of Science:
- Immunology
- Neurovirology
Background:
- The role of Interleukin-22 (IL-22), a Th17 cytokine, in viral infections remains largely unknown.
- IL-22 is primarily recognized for its role in host defense against extracellular pathogens.
Purpose of the Study:
- To investigate the role of IL-22 in West Nile virus (WNV) encephalitis.
- To elucidate the mechanisms by which IL-22 influences WNV pathogenesis in the central nervous system (CNS).
Main Methods:
- Utilized knockout mice lacking the Il22 gene (Il22(-/-)) and wild-type (WT) littermates.
- Assessed viral loads, leukocyte infiltration, cytokine expression, and apoptosis in the CNS following WNV infection.
- Quantified chemokine receptor (Cxcr2) expression on leukocytes and Cxcr2 ligand expression (cxcl1, cxcl5) in brain tissue.
Main Results:
- Il22(-/-) mice exhibited increased resistance to lethal WNV encephalitis compared to WT mice.
- Reduced viral loads, leukocyte infiltration, pro-inflammatory cytokines, and apoptosis were observed in the CNS of Il22(-/-) mice.
- Neutrophil migration into the CNS was significantly attenuated in Il22(-/-) mice, correlated with reduced Cxcr2 expression on leukocytes and lower Cxcr2 ligand levels in the brain.
Conclusions:
- IL-22 signaling exacerbates lethal WNV encephalitis.
- IL-22 likely promotes WNV neuroinvasion by enhancing neutrophil recruitment to the CNS.
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