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Necrotic 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 caecal tonsils (CT), bursa of Fabricius, Harderian gland (HG) and spleen tissues of broiler chickens infected with four  netB +  C. perfringens  strains (CP1, CP5, CP18, and CP26), of which CP18 and CP26 strains also carried the  tpeL  gene. The gross and histopathological 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-infected or uninfected chickens. Furthermore, CP26 infection also led to 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 the CP26-infected group compared to uninfected controls, 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.

avian pathology

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