Objective: Intestinal inflammatory diseases significantly affect animal health, primarily by disrupting intestinal barrier function. Indole-3-carboxaldehyde (IAld), a key metabolite of tryptophan derived from gut microbiota, exhibits protective properties against intestinal inflammatory diseases. The regulatory mechanism by which IAld modulates intestinal barrier function requires further investigation.Methods: An intestinal epithelial cell injury model was established by tumor necrosis factor-alpha (TNF-α) stimulation, alongside a mouse colitis model induced by dextran sulfate sodium (DSS) administration. Intestinal barrier function was assessed by immunoblotting, immunofluorescence, in vitro permeability assays, and histopathological analysis. Mitochondrial integrity and function were evaluated using JC-1 staining and transmission electron microscopy. Additionally, key components of the aryl hydrocarbon receptor (AhR)/AMP-activated protein kinase (AMPK) signaling pathway were analyzed using immunoblotting, immunofluorescence, and immunoprecipitation techniques.Results: Our findings demonstrate that IAld treatment significantly enhanced tight junction protein expression in intestinal epithelial cells and effectively attenuated TNF-α-induced intestinal barrier injury. IAld activated cellular AMPK signaling, promoting autophagy, maintaining mitochondrial homeostasis, and ultimately improving intestinal barrier function. Importantly, the activation of AMPK signaling by IAld was found to be dependent on the AhR, as evidenced by the AhR-specific inhibitor CH-223191, which abolished both IAld-induced AMPK activation and enhancement of intestinal barrier integrity. Furthermore, in vivo< experiments confirmed that IAld ameliorated intestinal barrier dysfunction and mitochondrial damage in DSS-induced colitis mice, whereas pharmacological inhibition of AMPK largely abrogated these protective effects.Conclusion: Our findings demonstrate that IAld effectively preserves intestinal barrier integrity, highlighting its potential application in the treatment of intestinal inflammatory diseases in both animals and humans.

Broodiness is a natural maternal behavior exhibited by female poultry, characterized by increased time spent sitting on the nest, feather fluffing, decreased appetite, cessation of egg-laying, and incubation behavior. The broodiness characteristics of female poultry are primarily regulated by external environmental factors and internal factors (such as genetics and hormones), and are regulated at the organ, cell, and molecular levels. At the organ level, the hypothalamic-pituitary-ovarian (HPO) axis plays a crucial role in regulating broodiness behavior. At the cellular level, hypothalamic hormones (such as GnRH), pituitary hormones (such as PRL, FSH, and LH), and gonadal hormones (such as estrogen and progesterone) bind to corresponding receptors on the cell membrane, activating different signaling pathways to regulate the apoptosis and autophagy of granulosa cells (GCs), thereby influencing the occurrence of broodiness behavior. At the molecular level, broodiness behavior in avian species is a complex trait controlled by multiple genes, with epigenetics playing a key role in the regulation of gene expression. However, the exact regulatory mechanisms of how these factors affect the ovarian structure and function, and consequently lead to broodiness behavior, remain unclear. Therefore, this paper discussed the characteristics of poultry broodiness behavior, the morphological changes in the reproductive system before and after broodiness, and provided a review of the regulatory mechanisms at the organ, cellular, and molecular levels, aiming to provide a reference for future research on poultry broodiness.

Taihe Black-Bone Silky Fowl (SF) is a famous local breed in China, known for its high nutritional and medicinal value. However, its low egg-laying rate significantly limits its economic benefits. This study aims to explore the ovarian development status, as well as the changes in the transcriptome and chromatin accessibility landscape at different egg-laying stages of SF, in order to reveal the epigenetic regulatory mechanisms underlying ovarian development in laying hens. The results showed that during peak egg-laying, serum levels of follicle stimulating hormone (FSH), luteinizing hormone (LH), estradiol (E2), and progesterone (P4) in the SF were higher than in the other laying periods. Meanwhile, the serum and ovarian matrix total antioxidant capacity (T-AOC) level decreased with increasing age, whereas the ovarian matrix malondialdehyde (MDA) level showed the opposite trend. Compared to the late laying period, several genes related to ovarian development and reproductive hormone secretion, including TDRD5, CCNO, CYP17A1, BMP15, and STAR, were upregulated during the peak egg-laying period. Additionally, we identified key transcription factors (TF) associated with different egg-laying periods. Specific TF, such as Fli1, Etv2, and AT2G15740, linked to the peak egg-laying period, play significant roles in cell and tissue development. The specific transcription factor Nr5a2, associated with the late laying period, has been shown to inhibit E2 production. Furthermore, genes related to poultry reproductive performance, such as STAR and WNT4, were found to be regulated by specific distal enhancers in open chromatin regions (OCR). In conclusion, this study elucidated the dynamic changes in the transcriptome and chromatin accessibility landscape during ovarian development in SF at different egg-laying stages and highlighted key TF, including Fli1, Etv2, and Nr5a2, as well as essential genes like STAR and WNT4 that regulate ovarian development. These findings provide valuable insights into the regulatory mechanisms influencing egg-laying performance in SF and offer new strategies for improving ovarian follicle development and egg production performance in poultry.

Objective: Animals will experience energy deprivation processes such as moulting, clutching, migration and long-distance transportation under natural survival conditions and in production practices, and the body will trigger a series of adaptive metabolic changes during these processes. Fasting and refeeding after fasting can induce remodeling of nutrients and energy metabolism. This study aims to investigate the mechanisms by which the gut microbiota and liver of poultry respond to energy deprivation under specific conditions.Methods: Ninety 252-day-old laying hens were randomly divided into 3 groups: (1) fed ad libitum (control group); (2) fasted from day 13 to day 17 (fasting group); (3) fasted from day 1 to day 5, then refed on a specific feeding way (refeeding group). After that, the serum, liver, jejunum tissues, and cecum contents were sampled and sent for metabolome, transcriptome, morphology, and 16S rDNA sequencing analyses, respectively.Results: Results showed that food deprivation not only observably decreased the body weight, liver index, and the villus height and villus/crypt ratio of jejunum, but also significantly changed the gut microbiota compositions, serum metabolic profiles, and the hepatic gene expression patterns of laying hens, whereas these changes were effectively reversed by the following refeeding operation. At the same time, metabolome combined transcriptome analysis revealed that both serum differential metabolites and hepatic differential expressed genes (DEGs) were consistently enriched in the lipid and amino metabolism pathways, and strong correlations were synchronously found between the differential metabolites and both of the differential gut microbial genera and DEGs, suggesting the crosstalks among gut, liver and their resulting serum metabolic products.Conclusion: The results suggested that the organism might coordinate to maintain metabolic homeostasis under energy deprivation through a combination of changes in gut microbial composition and hepatic gene expression.

Photoperiod, a pivotal environmental clue, orchestrates animal growth, reproduction, and metabolism through circadian rhythm regulation. However, the regulatory mechanisms of photoperiod on bile acid metabolism in poultry remain unclear. In this study, eighty 132-day-old Taihe silky fowls were allocated to either a control photoperiod group (CP, 13 h of light [L]: 11 h of dark [D]) or long photoperiod group (LP, 17L: 7D) for 240 days, and multi-omics approaches were applied to decipher the molecular mechanisms of bile acid metabolism regulation by photoperiod. Biochemical assays showed that LP treatment significantly increased serum total bile acids (TBA), hepatic triglycerides (TG), and hepatic TBA levels (P < 0.05). Targeted metabolomic analysis revealed significantly elevated serum levels of TCA, Tα-MCA, Tω-MCA, TCDCA, CDCA and TLCA-3S in LP group (P < 0.05). 16S rDNA sequencing indicated that LP group dramatically reduced gut microbial alpha diversity (Chao1, ACE, Shannon; P < 0.05) and altered microbiota composition, with enriched Fusobacteriota and depleted Actinobacteriota and Spirochaetota at the phylum level (P < 0.05), and significantly increased Fournierella, Megamonas, Bacteroides and decreased Ruminococcus, Parabacteroides at the genus level (P < 0.05). Transcriptome analysis identified 395 differentially expressed genes (DEGs) enriched in primary bile acid biosynthesis, ABC transporters, bile secretion, peroxisome, and cholesterol metabolism pathways. Notably, genes involved in bile acid synthesis genes (CYP7A1, CYP7B1), secretion gene (AQP9), and transport gene (ABCG5) showed significant upregulation under LP conditions (P < 0.05). In vitro validation confirmed TCA dose-dependently enhanced ABCG5 expression in hepatocytes (P < 0.05). Collectively, our findings demonstrate that photoperiod modulates bile acid metabolism through gut microbiota remodeling and hepatic gene reprogramming, offering novel targets for metabolic intervention in poultry.