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Updated: Dec 29, 2025

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
Published on: September 26, 2013
IL-17A treatment influences murine susceptibility to experimental Riemerella anatipestifer infection
Paula Leona T Cammayo1, Cherry P Fernandez-Colorado2, Rochelle A Flores1
1College of Veterinary Medicine & Institute of Animal Medicine, Gyeongsang National University, Jinju, 52828, Republic of Korea.
Abstract:
Riemerella anatipestifer causes infectious disease and considerable economic loss in the duck industry worldwide. Our previous studies demonstrated an association between proinflammatory cytokine interleukin (IL)-17A and R. anatipestifer infection. Here, we provide evidence for IL-17A involvement in R. anatipestifer infection using a mouse model. Mice showed higher resistance to R. anatipestifer infection than ducks, with median lethal doses (LD50) of 3.5 × 1010 and 5 × 107 colony-forming units (CFU), respectively. Twenty-four hours after infection, mice with a sub-lethal dose (3.5 × 109 CFU) exhibited levels of IL-17A and IL-23 expression similar to uninfected mice. Thus, we hypothesized that exogenous IL-17A or IL-23 administration affects susceptibility of mice to R. anatipestifer. Mice pretreated with IL-17A or IL-23 prior to sub-lethal dose infection of R. anatipestifer exhibited increased bacterial burden and spleen weights compared to untreated infected mice, confirming the involvement of IL-17A in susceptibility to R. anatipestifer infection in vivo.

