Mucosal and systemic lymphoid immune responses against Clostridium perfringens strains with variable virulence in the production of necrotic enteritis in broiler chickens.

AbstractNecrotic enteritis (NE), caused by Clostridium perfringens, is an economically important disease of chickens. Although NE pathogenesis is moderately well-studied, the host immune responses against C. perfringens are poorly understood. The present study used an experimental NE model to characterize lymphoid immune responses in the cecal tonsils (CT), bursa of Fabricius, Harderian gland (HG) and splenic tissues of broiler chickens infected with four netB + C. perfringens strains (CP1, CP5, CP18, and CP26), of which CP18 and CP26 strains also carried tpeL gene. The gross and histopathology lesions in chickens revealed CP5 to be avirulent, while CP1, CP18, and CP26 strains were virulent with CP26 being 'very virulent'. Gene expression analysis showed that while the virulent strains induced a significantly upregulated expression of pro-inflammatory IL-1β gene in CT, the CP26-infected birds had significantly higher CT transcription of IFNγ and IL-6 pro-inflammatory genes compared to CP5 or uninfected chickens. Furthermore, CP26-infection also led to a significantly increased bursal and HG expression of the anti-inflammatory/regulatory genes, IL-10 or TGFβ, compared to control, CP5 and CP1 groups. Additionally, the splenic pro- and anti-inflammatory transcriptional changes were observed only in the CP26-infected chickens. An antibody-mediated response, as characterized by increased IL-4 and/or IL-13 transcription and elevated IgM levels in birds infected with virulent strains, particularly in CP26-infected group compared to uninfected control, was also evident. Collectively, our findings suggest that lymphoid immune responses during NE in chickens are spatially regulated such that the inflammatory responses against C. perfringens depend on the virulence of the strain.