Background: Intestinal inflammation is prevalent in chicken, which results in decreased growth performance and considerable economic losses. Accumulated findings established the close relationship between gut microbiota and chicken growth performance. However, whether gut microbiota impacts chicken growth performance by lessening intestinal inflammation remains elusive. Results: Seven-weeks-old male and female chickens with the highest or lowest body weights were significantly different in breast and leg muscle indices and average cross-sectional area of muscle cells. 16S rRNA gene sequencing indicated Gram-positive bacteria, such as Lactobacilli, were the predominant species in high body weight chickens. Conversely, Gram-negative bacteria, such as Comamonas, Acinetobacter, Brucella, Escherichia-Shigella, Thermus, Undibacterium, and Allorhizobium-Neorhizobium-Pararhizobium-Rhizobium were significantly abundant in low body weight chickens. Serum lipopolysaccharide (LPS) level was significantly higher in low body weight chickens (101.58 ± 5.78 ng/mL) compared with high body weight chickens (85.12 ± 4.79 ng/mL). The expression of TLR4, NF-κB, MyD88, and related inflammatory cytokines in the jejunum was significantly upregulated in low body weight chickens, which led to the damage of gut barrier integrity. Furthermore, transferring fecal microbiota from adult chickens with high body weight into 1-day-old chicks reshaped the jejunal microbiota, mitigated inflammatory response, and improved chicken growth performance. Conclusions: Our findings suggested that jejunal microbiota could affect chicken growth performance by mitigating intestinal inflammation.

Cecal microbiota plays an essential role in chicken health. However, its contribution to fat metabolism, particularly in abdominal fat deposition, which is a severe problem in the poultry industry, is still unclear. Here, chickens at 1, 4, and 12 months of age with significantly (p < 0.05) higher and lower abdominal fat deposition were selected to elucidate fat metabolism. A significantly (p < 0.05) higher mRNA expression of fat anabolism genes (ACSL1, FADS1, CYP2C45, ACC, and FAS), a significantly (p < 0.05) lower mRNA expression of fat catabolism genes (CPT-1 and PPARα) and fat transport gene APOAI in liver/abdominal fat of high abdominal fat deposition chickens indicated that an unbalanced fat metabolism leads to excessive abdominal fat deposition. Parabacteroides, Parasutterella, Oscillibacter, and Anaerofustis were found significantly (p < 0.05) higher in high abdominal fat deposition chickens, while Sphaerochaeta was higher in low abdominal fat deposition chickens. Further, Spearman correlation analysis indicated that the relative abundance of cecal Parabacteroides, Parasutterella, Oscillibacter, and Anaerofustis was positively correlated with abdominal fat deposition, yet cecal Sphaerochaeta was negatively correlated with fat deposition. Interestingly, transferring fecal microbiota from adult chickens with low abdominal fat deposition into one-day-old chicks significantly (p < 0.05) decreased Parabacteroides and fat anabolism genes, while markedly increased Sphaerochaeta (p < 0.05) and fat catabolism genes (p < 0.05). Our findings might help to assess the potential mechanism of cecal microbiota regulating fat deposition in chicken production.

Background: Intestinal inflammation has become a threatening concern in chicken production worldwide and is closely associated with Th17/Treg cell imbalance. Several studies described that gut microbiota is significantly implicated in chicken growth by modulating intestinal immune homeostasis and immune cell differentiation. Whether reshaping gut microbiota by fecal microbiota transplantation (FMT) could improve chicken growth by balancing Th17/Treg cells is an interesting question. Results: Here, the chickens with significantly different body weight from three different breeds (Turpan cockfighting × White Leghorn chickens, white feather chickens, and yellow feather chickens) were used to compare Th17 and Treg cells. qPCR and IHC staining results indicated that Th17 cell-associated transcriptional factors Stat3 and rorγt and cytokines IL-6, IL-17A, and IL-21 were significantly (P < 0.05) higher in the jejunum of low body weight chickens, while Treg cell-associated transcriptional factor foxp3 and cytokines TGF-β and IL-10 were significantly (P < 0.05) lower in the jejunum of low body weight chickens, indicating imbalanced Th17/Treg cells were closely related to chicken growth performance. Transferring fecal microbiota from the healthy donor with better growth performance and abundant Lactobacillus in feces to 1-day-old chicks markedly increased growth performance (P < 0.001), significantly decreased Th17 cell-associated transcriptional factors and cytokines, and increased Treg cell-associated transcriptional factors and cytokines in the jejunum (P < 0.05). Furthermore, FMT increased the abundance of Lactobacillus (FMT vs Con; 84.98% vs 66.94%). Besides, the metabolites of tryptophan including serotonin, indole, and 5-methoxyindoleacetate were increased as well, which activated their receptor aryl-hydrocarbon-receptor (AhR) and expressed more CYP1A2 and IL-22 to maintain Th17/Treg cell balance and immune homeostasis. Conclusion: These findings suggested that imbalanced Th17/Treg cells decreased chicken growth performance, while FMT-reshaped gut microbiota, i.e., higher Lactobacilli, increased chicken growth performance by balancing Th17/Treg cells.

Probiotics can promote the health and growth performance of animals through modulation of intestinal microbiota. When used as a feed additive, they have the potential to minimize or abolish the use of antibiotics. In this study, we investigated the effect of the probiotic strainBacillus amyloliquefaciensTL on the growth performance and cecum microflora composition in Cobb 500 broiler chickens. In total, 180 broilers were randomly divided into three groups—each group comprised 4 pens, and each pen contained 15 chickens. The three groups were fed either a control diet, or a diet supplemented with either the antibiotic chlortetracycline orB. amyloliquefaciensTL. Broilers were weighed, and cecum contents were collected on days 7, 14, 21, and 35, respectively. The broilers in both the antibiotic and probiotic groups exhibited significant weight gain compared with controls, exhibiting increases of 16.02% and 13.40%, respectively, after 35 days (P<0.01). Similarly, the feed conversion ratio (FCR, 1–35 days) of broilers in the chlortetracycline andB. amyloliquefaciensTL groups was lower than that of the controls. HiSeq high-throughput sequencing of 16S rRNA of the cecal microbiota was performed on days 7, 14, 21, and 35, respectively. TheFirmicutes/Bacteroidetesratio was higher in the chlortetracycline andB. amyloliquefaciensTL groups than in the control group on days 14, 21, and 35, and especially on day 21. The prevalence of generaOscillospira,Ruminococcus,Butyricicoccus, andFaecalibacterium(Firmicutes) was higher in the antibiotic and probiotic groups, while that ofBacteroides,Parabacteroides(Bacteroidetes), andLactobacilluswas higher in the control group. In this study, the changes in the microbiota of the probiotic group were similar to those in the antibiotic group. These results suggest that the probiotic strainB. amyloliquefaciensTL can modulate the cecal microbiota of broilers similar to chlortetracycline.

Mastitis is an emerging health concern in animals. An increased incidence of mastitis in dairy cows has been reported in the last few years across the world. It is estimated that up to 20% of cows are suffering from mastitis, causing incompetency in the mucosal immunity and resulting in excessive global economic losses in the dairy industry. Staphylococcus aureus (S. aureus) has been reported as the most common bacterial pathogen of mastitis at clinical and sub-clinical levels. Antibiotics, including penicillin, macrolides, lincomycin, cephalosporins, tetracyclines, chloramphenicol, and methicillin, were used to cure S. aureus-induced mastitis. However, S. aureus is resistant to most antibiotics, and methicillin-resistant S. aureus (MRSA) especially has emerged as a critical health concern. MRSA impairs immune homeostasis leaving the host more susceptible to other infections. Thus, exploring an alternative to antibiotics has become an immediate requirement of the current decade. Short chain fatty acids (SCFAs) are the potent bioactive metabolites produced by host gut microbiota through fermentation and play a crucial role in host/pathogen interaction and could be applied as a potential therapeutic agent against mastitis. The purpose of this review is to summarize the potential mechanism by which SCFAs alleviate mastitis, providing the theoretical reference for the usage of SCFAs in preventing or curing mastitis.

The probioticEnterococcus faeciumHDRsEf1 (Ef1) has been shown to have positive effects on piglet diarrhoea, but the mechanism has not yet been elucidated. In this study, using the IPEC-J2 cell line to mimic intestinal epithelial cells and enterotoxigenicEscherichia coli(ETEC) K88ac as a representative intestinal pathogen, the mechanism underlying Ef1 protection against an enteropathogen was investigated. The results demonstrated that Ef1 was effective in displacing K88ac from the IPEC-J2 cell layer. Moreover, Ef1 and its cell-free supernatant (S-Ef1) modulate IL-8 released by IPEC-J2 cells. Ef1 and its cell-free supernatant showed the potential to protect enterocytes from an acute inflammatory response. In addition, Ef1 and its cell-free supernatant increased the transepithelial electrical resistance (TEER) of the enterocyte monolayer, thus strengthening the intestinal barrier against ETEC. These results may contribute to the development of therapeutic interventions using Ef1 in intestinal disorders of piglets.