Abstract
Necrotic enteritis (NE), mainly induced by the pathogens of Clostridium perfringens and coccidia, causes huge economic losses with limited intervention options in the poultry industry. This study investigated the role of specific bile acids on NE development. Day-old broiler chicks were assigned to six groups: noninfected, NE, and NE with four bile diets of 0.32% chicken bile, 0.15% commercial ox bile, 0.15% lithocholic acid (LCA), or 0.15% deoxycholic acid (DCA). The birds were infected with Eimeria maxima at day 18 and C. perfringens at day 23 and 24. The infected birds developed clinical NE signs. The NE birds suffered severe ileitis with villus blunting, crypt hyperplasia, epithelial line disintegration, and massive immune cell infiltration, while DCA and LCA prevented the ileitis histopathology. NE induced severe body weight gain (BWG) loss, while only DCA prevented NE-induced BWG loss. Notably, DCA reduced the NE-induced inflammatory response and the colonization and invasion of C. perfringens compared to NE birds. Consistently, NE reduced the total bile acids in the ileal digesta, while dietary DCA and commercial bile restored it. Together, this study showed that DCA and LCA reduced NE histopathology, suggesting that secondary bile acids, but not total bile acid levels, play an essential role in controlling the enteritis.
Highlights
Accepted: 13 August 2021Clostridium perfringens, a spore-forming, anaerobic, and Gram-positive bacterium, is an opportunistic gut pathogen which causes necrotic enteritis (NE), a prevalent chicken disease [1,2,3]
Cell death is categorized into accidental cell death and regulated cell death (RCD), and some of the RCDs are apoptosis, necrosis, necroptosis, and pyroptosis [25]. It remains largely elusive which death pathways are activated in NE, we have reported that apoptosis is present in the enteritis [1]
To evaluate the mechanism of deoxycholic acid (DCA) and lithocholic acid (LCA) that was improving the NE signs, we examined the impact of the dietary bile acids on NE at the cellular level using a histopathology analysis
Summary
Clostridium perfringens, a spore-forming, anaerobic, and Gram-positive bacterium, is an opportunistic gut pathogen which causes necrotic enteritis (NE), a prevalent chicken disease [1,2,3]. NE is estimated to be responsible for losses of around USD six billion in the poultry industry worldwide every year [4]. The increased NE incidence is associated with the increasing restriction of prophylactic antimicrobial supplementation in farm animal production in the absence of effective alternatives [5]. Despite its largely elusive pathogenesis, NE at poultry farms is frequently intercurrent with the infections of coccidia such as Eimeria maxima and E. acervuline [6]. To mimic the enteritis in field conditions, the NE animal model is often a co-infection of E. maxima and C. perfringens [7]. Investigators have successfully induced a natural NE by placing birds in rooms exposed to previous
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