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.

Objectives: Obesity is associated with cardiac remodeling characterized by cardiomyocyte hypertrophy and fibrosis, eventually leading to heart failure. This study aimed to evaluate whether dietary matcha supplementation could be effective in reducing high-fat, high-sugar diet (HFD)-induced cardiac remodeling in mice, and whether this effect is linked to changes in the gut microbiota along the gut–heart axis. Methods: Six-week-old C57BL/6J mice were randomly divided into normal chow diet (NCD) or HFD (without matcha, 0.2% matcha, or 1% matcha) groups. Dietary intervention continued for 10 weeks with continuous monitoring of body weight. After completion of the intervention, hearts were collected, weighed, and processed for histological examination of cardiomyocyte size with wheat germ agglutinin (WGA) staining and collagen deposition with Picrosirius Red staining. The gut microbiome was evaluated using 16S rRNA sequencing of gDNA from feces, and correlation analysis was performed between microbial taxa and cardiometabolic parameters. Results: After 10 weeks of dietary intervention, heart weight was significantly lower in mice treated with 1% matcha than in HFD controls. WGA staining showed a significant increase in cardiomyocyte size in the HFD group compared with the NCD group, whereas both the 0.2% and 1% matcha-supplemented groups revealed significantly smaller cardiomyocytes than the HFD controls. In addition, both matcha doses significantly reduced cardiac collagen deposition relative to HFD controls. In the gut, matcha supplementation displayed a marked increase in the abundance of beneficial gut microbiota, including Ligilactobacillus, Lactobacillus, and Oscillospiraceae, while reducing pathogenic Enterobacteriaceae and Klebsiella, particularly at the high dose. Conclusions: Dietary matcha supplementation attenuated HFD-induced cardiac hypertrophy and fibrosis in mice, independently of body weight, in association with modulation of the gut microbiota along the gut–heart axis. Future studies should determine whether the observed reductions in cardiac hypertrophy and fibrosis translate into measurable improvements in cardiac function and whether the associated gut microbiota alterations exert causal effects on cardiac remodeling.