Iron is a vital trace element that plays an important role in humans and other organisms. It plays an active role in the growth, development, and reproduction of bacteria, such as Bifidobacteria. Iron deficiency or excess can negatively affect bacterial hosts. Studies have reported a major role of iron in the human intestine, which is necessary for maintaining body homeostasis and intestinal barrier function. Organisms can maintain their normal activities and regulate some cancer cells in the body by regulating iron excretion and iron-dependent ferroptosis. In addition, iron can modify the interaction between hosts and microorganisms by altering their growth and virulence or by affecting the immune system of the host. Lactic acid bacteria such as Lactobacillus acidophilus (L. acidophilus), Lactobacillus rhamnosus (L. rhamnosus), and Lactobacillus casei (L. casei) were reported to increase trace elements, protect the host intestinal barrier, mitigate intestinal inflammation, and regulate immune function. This review article focuses on the two aspects of the iron and gut and generally summarizes the mechanistic role of iron ions in intestinal immunity and the remodeling of gut microbiota.

Different rearing systems have varying effect on animal welfare and meat quality of poultry. Currently, there are no established standards for the rearing systems of Chinese indigenous chickens. Our study aimed to investigate the effects of different rearing systems on the meat quality, gene profiles, and metabolites of Chinese indigenous chickens (Nanchuan chicken). 10-wk-old Nanchuan chickens (n=360) were randomly divided into 3 groups (cage, net, and free-range groups), with 6 replicates per group (20 chickens per replicate). The experiment lasted for 12 wk. At 154-days-old, 36 healthy chickens (6 males and 6 females per group) were randomly selected, euthanized, and their breast muscles were collected to assess the meat quality parameters and histomorphological characteristics. Additionally, breast muscles from 18 random hens (3 males and 3 females per group) were used for metabolomics and RNA-seq analysis. The results showed that rearing systems significantly affected the meat quality and myofiber characteristics. The meat quality of breast muscles from free-range chickens was superior to that of caged chickens, characterized by more tender meat and smaller myofiber cross-sectional areas. Integrative metabolomics and transcriptomics analysis revealed that the differentially expressed genes of chicken breast muscles were primarily involved in the myofiber differentiation. Mechanically, the improved meat quality of breast muscle in free-range chickens were mainly associated with enhanced skeletal muscle differentiation facilitated by fibromodulin, increased levels of up-regulated Acetyl-L-carnitine and Propionylcarnitine level, and decreased levels of Nonanoic acid and Elaidic acid abundance (Graphical abstract). This provides a comprehensive understanding of the most effective and sustainable breeding, production, and rearing systems for Chinese indigenous chickens. It also contributes to the current knowledge of the molecular mechanisms underlying the effects of rearing systems on growth performance and meat quality of chickens.

The development of pre-recruitment follicles plays a critical role in determining egg-laying performance in poultry. This study combines proteomic and metabolomic analyses to explore changes in proteins and metabolites, to elucidate key regulatory mechanism involved in chicken pre-recruitment follicular development. Histological examination revealed a significant increase in yolk deposition in small yellow follicles (SYF) compared to small white follicles (SWF). Metabolomics analysis identified significantly enriched differential metabolites (DMs) between SWF and SYF in pathways such as Lysosome, Ferroptosis, Biosynthesis of unsaturated fatty acids, and Tryptophan metabolism. Particularly, Adenosine-5'-Diphosphate (ADP) was downregulated during follicular recruitment and was significantly enriched in the lysosome pathway. Proteomic analyses revealed that differentially expressed proteins (DEPs) in SWF and SYF were enriched in pathways including Lysosome, Glutathione metabolism, Cholesterol metabolism, Arginine and proline metabolism, and amino acid biosynthesis. Among these DEPs, NAD-dependent protein deacetylase sirtuin 5 (SIRT5) was significantly upregulated, while lysosomal-associated membrane protein 1 (LAMP1) was down-regulated during the development of pre-recruitment follicles. SIRT5 was linked to the negative regulation of reactive oxygen species metabolism, whereas LAMP1 was associated with lysosome and autophagy pathways. Further validation experiments demonstrated high expression of SIRT5 in SYF, particularly in granulosa cells (GCs). Silencing SIRT5 in GCs resulted in increased ROS production and upregulated expression of autophagy-related proteins LC3Ⅱ and Beclin1, as well as lysosome markers LAMP1. Conversely, lipid droplet deposition and p62 expression were suppressed. inhibited. Taken together, these findings suggest that SIRT5 upregulation promotes the development of pre-recruitment follicles by inhibiting the autophagy-lysosome pathway in chicken GCs.

Reproductive efficiency forms the cornerstone of poultry production, yet ovarian oxidative stress and brooding that emerge with advancing age accelerate follicular atresia, leading to ovarian atrophy. This subsequently disrupts ovulation and shortens the laying cycle. Despite its economic implications, the molecular mechanisms linking these processes to granulosa cell (GC) fate remain poorly understood. This study aimed to construct ceRNA regulatory networks and unravel how microRNA-30b-5p (miR-30b-5p) and its target gene nuclear receptor subfamily 5 group A member 2 (NR5A2) regulate GC proliferation and apoptosis in chicken atrophic ovaries. In this study, we found that the ovarian tissue undergoes degeneration, with reduced levels of the hormones follicle-stimulating hormone (FSH) and luteinizing hormone (LH), and a significant decrease in ovarian antioxidant activity of broody chickens. Whole-transcriptome sequencing on atrophic ovaries (AO) from 700-day-old Hy-line Gray broody hens and normal ovaries (NO) from actively laying hens identified 260 differentially expressed (DE) lncRNAs, 492 DE circRNAs, 53 DE miRNAs, and 4,493 DE mRNAs. Further, integrative analysis revealed miR-30b-5p as a candidate regulator of GC proliferation and apoptosis. Additionally, functional assays including RT-qPCR, western blotting, flow cytometry, cell counting kit 8 (CCK-8) and 5-ethynyl-20-deoxyuridine (EdU) assay incorporation demonstrated that miR-30b-5p overexpression suppressed GC proliferation (reduced CDK2, Cyclin D1, PCNA, and Bcl-2) and promoted apoptosis (increased Caspase-3 and Caspase-9). Thereafter, target prediction and dual-luciferase reporter assays further confirmed that NR5A2 as a direct target of miR-30b-5p, and that NR5A2 knockdown phenocopied the anti-proliferative and pro-apoptotic effects of miR-30b-5p. Taken together, the findings obtained from this study demonstrate that miR-30b-5p promotes GC apoptosis and inhibits proliferation by targeting NR5A2, thereby contributing to follicular atresia during broodiness in the late laying phase. Targeted modulating of miR-30b-5p may offer a promising strategy to alleviate ovarian atrophy, extend the laying cycle and enhance economic efficiency in poultry production.