Analysis of immunomodulation to intestinal inflammatory injury in chickens caused by Clostridium perfringens C57-1 infection

Abstract By releasing a variety of toxins and invasive enzymes, Clostridium perfringens ( C. perfringens ) attached to the intestinal epithelium triggers receptors on intestinal target cells and activates intracellular signalling pathways, resulting in intestinal inflammation and immunological responses. We developed a model of experimental induction of necrotic enteritis (NE) in chickens in order to investigate the intestinal immunomodulatory to inflammatory damage caused by C. perfringens type A C57-1 infection. Growth rate and feed intake of the challenged chickens reduced, and the intestinal mucosa had varying degrees of injury and necrosis along with widespread inflammatory infiltration. The relative abundance of Lactobacillus was significantly reduced in the challenged intestine compared to the control, while the level of Clostridiales , Bacteroidales , and Erysipelotrichales increased. The activity of the β-glucuronidase and β-glucosidase enzymes in the challenged chickens was also significantly higher. The Th17/Treg balance in the gut was upset, and the proinflammatory cytokines IL-17 and IL-1β and IL-13 also elevated dramatically, which together synergistically induced inflammation. As the inflammation intensified, TGF-4 and IL-2 levels in the gut of the challenge group fell at first and then moderately recovered in comparison to the control group. Immunomodulated by Th2 and Th17 immunity, the challenged chickens were able to produce specific IgY against C. perfringens C57-1, thus exerting limited anti-inflammatory effects. From the standpoint of immunological prevention, this study established a theoretical foundation for C. perfringens infection.