Heat stress has emerged as a serious threat to the global poultry industry due to climate change. Heat stress can negatively impact the growth, gut health, immune function, and production and reproductive performances of poultry. Different strategies have been explored to mitigate heat stress in poultry; however, only a few have shown potential. Probiotics are gaining the attention of poultry nutritionists, as they are capable of improving the physiology, gut health, and immune system of poultry under heat stress. Therefore, application of probiotics along with proper management are considered to potentially help negate some of the negative impacts of heat stress on poultry. This review presents scientific insight into the impact of heat stress on poultry health and growth performance as well as the application of probiotics as a promising approach to alleviate the negative effects of heat stress in poultry.

The rise of antimicrobial resistance has created an urgent need for antibiotic-alternative strategies for disease control and prevention. Host defense peptides (HDPs), which have both antimicrobial and immunomodulatory properties, are an important component of the innate immune system. A host-directed approach to stimulate the synthesis of endogenous HDPs has emerged as a promising solution to treat infections with a minimum risk for developing antimicrobial resistance. Among a diverse group of compounds that have been identified as inducers of HDP synthesis are polyphenols, which are naturally occurring secondary metabolites of plants characterized by the presence of multiple phenol units. In addition to their well-known antioxidant and anti-inflammatory activities, a variety of polyphenols have been shown to stimulate HDP synthesis across animal species. This review summarizes both the in vitro and in vivo evidence of polyphenols regulating HDP synthesis. The mechanisms by which polyphenols induce HDP gene expression are also discussed. Natural polyphenols warrant further investigation as potential antibiotic alternatives for the control and prevention of infectious diseases.

The intestinal microbiota is known to be altered by Eimeria-induced coccidiosis, but it remains unclear whether the microbiota is fully restored after recovery. To address this, 110 newly hatched Cobb male broiler chickens were challenged with 2 × 10⁴ sporulated oocysts of Eimeria maxima (EM) strain M6 or mock-infected with saline on day 10. Body weight and feed intake were recorded. Additionally, 10 mock- and 12 EM-infected birds were randomly selected to assess the small intestinal lesion, fecal oocyst shedding, and ileal and cecal microbiota compositions using 16S rRNA gene sequencing at 3, 5, 7, 14, and 21 days post-infection (dpi). EM infection significantly decreased (p < 0.001) body weight by 5 dpi, persisting through 21 dpi. The infection also reduced (p < 0.05) weight gain, feed intake, and feed efficiency in the first week; however, these parameters became comparable in the second and third weeks. At 7 dpi, during the peak of infection, major lactic acid bacteria were enriched, while short-chain fatty acid-producing bacteria were mostly suppressed in both the ileum and cecum. Opportunistic pathogens such as Escherichia and Clostridium perfringens transiently bloomed at 7 dpi. By 14 dpi, differential bacterial enrichment subsided, and nearly all commensal bacteria returned to healthy levels by 21 dpi. Coupled with comparable growth performance between healthy and EM-recovered chickens, we conclude that the intestinal microbiota is largely restored to its healthy state after recovery. Understanding the microbiota’s responses to coccidiosis may inform probiotic-based mitigation strategies.

Necrotic enteritis (NE), caused by Clostridium perfringens, poses significant economic challenges to the global poultry industry. The widening ban on in-feed antibiotics in livestock production underscores the need for alternative strategies to combat NE. Deoxycholic acid (DCA), a secondary bile acid, has shown promise in NE mitigation. However, its protective mechanism remains largely unexplored. A total of 120 newly hatched, male Cobb broilers were randomly divided into four treatments to investigate the impact of DCA on host response and intestinal microbiome in both healthy and NE-infected chickens. The results demonstrated that the dietary supplementation of 1.5 g/kg DCA significantly improved animal survival, reversed growth inhibition, and alleviated intestinal lesions (p < 0.01). Furthermore, DCA selectively inhibited the NE-induced proliferation of C. perfringens and other pathobionts such as Escherichia and Enterococcus cecorum. Concurrently, DCA markedly enriched dominant lactic acid bacteria like Lactobacillus johnsonii in both the ileum and cecum of NE-infected chickens. However, DCA had a marginal effect on the jejunal transcriptomic response in both mock- and NE-infected chickens. Therefore, we conclude that DCA protects chicken from NE mainly through the targeted inhibition of pathobionts including C. perfringens, with minimum impact on the host. These findings elucidate the protective mechanisms of DCA, supporting its development as a promising antibiotic alternative for NE mitigation.