Upregulation of duck interleukin-17A during Riemerella anatipestifer infection

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“…Gene expression was quantified using the comparative ΔΔCT method, with β-actin as a reference for normalization. The fold change in expression of each gene examined from R. anatipestifer-infected birds and in vitro-stimulated cells was calculated relative to the expression level in the same tissue or cells from uninfected or unstimulated samples, as previously described [15,42,49].…”

“…Our previous studies indicated that bacterial burden during R. anatipestifer infection in ducks is the highest on day 4 post-infection [15,16]. Therefore, the bacterial load in the livers and spleens of infected/treated ducks was determined on day 4 post-infection.…”

“…DIM supressed Th17 cell differentiation, resulting in downregulation of IL-17A expression levels [25]. Our previous studies demonstrated upregulated expression of inflammatory cytokines, including IL-17A, in R. anatipestifer-infected ducks [15,42,47]. Thus, the expression mRNA were normalized to that of β-actin and calibrated using the expression levels of unstimulated cultured splenic lymphocytes (NC).…”

“…Ducks vaccinated with inactivated R. anatipestifer plus levamisole as an adjuvant showed increased secretion of Th1-type (interferon [IFN]-γ and interleukin [IL]-2) and Th2-type (IL-4 and IL-10) cytokines and enhanced survival following challenge infection with a homologous R. anatipestifer strain [14]. Recent comparative analyses of the expression of immune-related genes between ducks and chickens revealed significantly higher IL-17A levels in both R. anatipestifer-infected ducks and killed R. anatipestifer-stimulated splenic lymphocytes [15,16]. Mice pre-treated with IL-17A or IL-23 prior to infection with R. anatipestifer at a sub-lethal dose exhibited increased bacterial burden and spleen weight compared to untreated infected mice [17].…”

“…The Th17 family of cytokines (IL-17A-F) has attracted attention due to its broad range of biological activities against pathogens [18,19]. IL-17A plays a particularly important role in host defense against infection with pathogens such as Staphylococcus aureus and Citrobacter rodentium [20], Chlamydia muridarum [21], and R. anatipestifer [15,16]. The critical involvement of Th1 and Th17 cells in the pathogenesis of various diseases has been demonstrated in a number of studies, and successful suppression of disease development is believed to involve neutralization or suppression of Th1 and Th17 cells [22][23][24].…”