Characterization of intestinal immune response to clostridium perfringens infection in broiler chickens characterization of intestinal immune tesponse to clostridium perfringens infection in broiler chickens

Authors: FASINA, YEWANDE - North Carolina Agricultural And Technical State University; Lillehoj, Hyun

Submitted to: Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/2/2018
Publication Date: 8/2/2018
Citation: Fasina, Y.O., Lillehoj, H.S. 2018. Characterization of intestinal immune response to clostridium perfringens infection in broiler chickens characterization of intestinal immune tesponse to clostridium perfringens infection in broiler chickens. Poultry Science. 98:188-198.

Interpretive Summary: Necrotic enteritis is caused by Clostridium perfringens (CP) bacteria which produces toxins. Understanding host immune response to CP is important to develop an effective strategy against NE which is costing more than $6 billion annual economic loss. In this report, ARS scientist and Our results clearly show that various cytokines and their associated immune function(s) are affected by CP infection. Plasma antibody levels to CP were also affected. Necrotic enteritis toxin B (NetB)-producing Clostridium perfringens (CP) is etiological agent of necrotic enteritis (NE) - an economically significant disease in broiler chickens. Understanding North Carolina University scientist collaborated to find the nature of intestinal host response. It was concluded that CP-infection induced inflammatory response in the intestine of broiler chickens. In summary, downregulation of TGF-ß, along with a concurrent upregulation in IL-1ß, IL-13, and IL-17 indicate that CP-induced subclinical NE triggered inflammatory immune response in the intestine of broiler chicks. In addition, the presence of higher levels of antibodies to recombinant CP proteins in challenged PCX and PCM treatments (P < 0.05), compared to the unchallenged CX and CM corroborates the cytokine gene expression results. It was concluded that the signaling mechanisms underlying the inflammatory response to intestinal CP infection are probably modulated by Th2 and Th17 cells. Furthermore, these results suggest that any future strategies to reduce the negative effects of NE should be selected based on their potential to induce Th2 and Th17 cytokine secretion.

Technical Abstract: Necrotic enteritis toxin B (NetB)-producing Clostridium perfringens (CP) is etiological agent of necrotic enteritis (NE) - an economically significant disease in broiler chickens. Understanding the immune response to CP infection in broiler chickens is becoming important to developing effective vaccines against NE. An experiment was conducted to determine the expression levels of selected cytokine genes in the intestine and cecal tonsil of CP-challenged broiler chickens. In a floor-pen housing, broiler chickens were randomly assigned to the following treatment groups; 1) bacitracin methylene disalicylate (BMD)-free control diet with no CP challenge (CX), 2) BMD-supplemented diet with no CP challenge (CM), 3) BMD-free control diet with CP challenge (PCX), or 4) BMD-supplemented diet with CP challenge (PCM). The establishment of CP infection was confirmed, with the treatment groups exposed to CP having a 1.5 to 2-fold higher CP levels (P < 0.05) compared to the non-exposed groups. On d 1 and 7 post-challenge, jejunal segments and cecal tonsils were collected from experimental chickens for quantitative real-time RT-PCR analysis to determine the expression levels of interleukin (IL)-1, interferon-' (IFN-'), IL-2, IL-13, IL-17, IL-10, and TGF-ß genes. Levels of antibodies to CP recombinant proteins were also determined in the plasma of experimental chickens. Results indicated that IL-1ß (pro-inflammatory cytokine), IL-13 (Th2 cytokine), and IL-17 (Th17 cytokine) were upregulated (P < 0.05) in CP-challenged PCX and PCM treatments, compared to the unchallenged (control) CX and CM treatments. A reverse trend was observed for TGF-ß (anti-inflammatory cytokine), while no change was observed in IFN-' (Th1 cytokine). It was concluded that CP-infection induced inflammatory response in the intestine of broiler chickens, and the mechanisms of inflammation are probably mediated via Th2 and Th17 cells.