Effects of DSS-induced intestinal disruption on egg quality and brain, liver, and ovarian follicle functions in laying hens

Intestinal disruptions, including morphological changes, barrier dysfunction, and inflammation, are associated with reduced egg production in laying hens. A previous study reported that oral administration of low-dose dextran sodium sulfate (DSS; 0.255 g/kg body weight) for 28 days caused slight intestinal disruption, resulting in decreased egg production and yolk size in the first week. These findings suggest that short-term DSS exposure may induce long-lasting effects on follicular development; however, the mechanisms underlying this early response remain unclear. This study aimed to investigate the mechanisms underlying the reduction in egg and yolk production during the first week. White Leghorn laying hens (350 days old) were divided into five groups: DSS-treated groups for 1 (DSS1), 2 (DSS2), and 7 (DSS7) consecutive days, and control groups receiving distilled water for 0 (CON0) and 7 (CON7) consecutive days. Egg parameters and serum corticosterone levels were assessed in the CON7 and DSS7 groups. At each time point, the birds were euthanized, and samples from the intestine, liver, granulosa cells (F1 and F5 follicles), hypothalamus, and pituitary gland were collected. Low-doses of DSS administration yielded the following results: (1) decreased claudin-1 (CLA-1) and claudin-5 (CLA-5) in the cecum in DSS1 and DSS2, while increased pro-inflammatory cytokines in the ileum and cecum in DSS2 and DSS7. (2) Increased sterol regulatory element binding protein-1 (SREBP-1), very low density lipoprotein-II (VLDL-II), and estrogen receptor alpha (Erα) in the liver in DSS7. (3) Decreased low-density lipoprotein receptor (LDLr) and lipoprotein receptor 8 (LR8) in the granulosa cells in DSS2, with increased CLA-1 and CLA-5 in DSS1; both patterns were reversed in DSS7. (4) Increased stress-related hormone synthesis in DSS1 and DSS7, and gonadotropin-releasing hormone (GnRH), luteinizing hormone (LH), and follicle stimulating hormone (FSH) gene expression in DSS1 and DSS2. These results suggest that slight intestinal disruption triggers a systemic stress response that impairs yolk precursor uptake and follicular function, leading to reduced egg weight and yolk size without affecting gonadotropin or yolk precursor production. After one week, a compensatory feedback response restored yolk precursor uptake and gonadotropin synthesis, but yolk size continued to decline. In conclusion, these findings suggest that short-term intestinal disruption serves as a key trigger for prolonged impairment of reproductive function and egg quality in laying hens.