Glaesserella parasuis induces IL-17 production might through PKC-ERK/MAPK and IκB/NF-κB signaling pathways

Xinyi He1, Xin Song1, Hui Cao1

  • 1College of Animal and Veterinary Sciences, Southwest Minzu University, Chengdu 610041, China.

Insights

Glaesserella parasuis infection significantly increases interleukin-17A (IL-17A) in piglets, particularly in lungs and spleens. This response is mediated by the activation of PKC-ERK/MAPK and IκB/NF-κB signaling pathways in macrophages.

Area of Science:

  • Veterinary Immunology
  • Bacterial Pathogenesis
  • Host-Pathogen Interactions

Background:

  • Previous studies identified the outer membrane protein P2 of Glaesserella parasuis (G. parasuis) as an inducer of interleukin-17A (IL-17A).
  • The precise mechanisms by which G. parasuis infection leads to IL-17A production in the host remained unclear.

Purpose of the Study:

  • To investigate the role of IL-17A in G. parasuis infection in piglets.
  • To elucidate the signaling pathways involved in G. parasuis-induced IL-17A production.

Main Methods:

  • Flow cytometry to assess Th17 cell proportions in peripheral blood.
  • Measurement of IL-17 mRNA and protein levels in lung and spleen tissues.
  • Histopathological examination, immunohistochemistry, and viability counts.
  • Infection of primary porcine alveolar macrophages (PAMs) with different G. parasuis strains.
  • Western blotting to analyze signaling pathway activation (PKC, ERK1/2, IκB).
  • Use of specific pathway inhibitors (PKC, MEK, NF-κB).

Main Results:

  • A significant increase in IL-17 mRNA and protein levels was observed in the lungs and spleens of infected piglets.
  • IL-17 expression correlated positively with bacterial load and pathological damage in tissues.
  • Primary PAMs produced significantly more IL-17 in a time- and dose-dependent manner when infected with virulent G. parasuis strains.
  • PKC, MEK, and NF-κB signaling pathways were identified as essential for G. parasuis-induced IL-17 production, as evidenced by reduced IL-17 mRNA levels upon inhibitor treatment.
  • Increased phosphorylation of PKC, ERK1/2, and IκB was observed in infected PAMs.

Conclusions:

  • G. parasuis infection triggers IL-17 production in piglets, primarily in the respiratory tract and spleen.
  • The activation of the PKC-ERK/MAPK and IκB/NF-κB signaling pathways is crucial for G. parasuis-induced IL-17 production.
  • IL-17 expression is linked to bacterial burden and disease severity in G. parasuis infections.

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