The role of visfatin in peripheral immune organs and intestines of weaned piglets under lipopolysaccharide induced immune stress.

To investigate the regulatory mechanisms and pathways of visfatin under immune stress injury in weaned piglets, we established a lipopolysaccharide-induced immune stress model in weaned piglets to study how visfatin affects peripheral immune organs and intestinal function. The results revealed that visfatin improved the inflammatory response in immune-stressed weaned piglets by reducing the levels of pro-inflammatory cytokines interleukin-1β, interleukin-6 and monocyte chemoattractant protein-1, as well as decreasing the neutrophil/lymphocyte ratio. Visfatin ameliorated oxidative stress in piglets by promoting the expression of superoxide dismutase and glutathione peroxidase. It also enhanced cell proliferation in peripheral immune organs (spleen and mesenteric lymph nodes) and suppressed cell apoptosis in these organs through the death receptor apoptosis pathway, thereby improving the immune function of weaned piglets under immune stress. Moreover, it alleviated intestinal villi damage, increased the abundance of beneficial bacteria, and elevated the levels of short-chain fatty acids, thus preserving the intestinal barrier's integrity and the balance of intestinal microbiota. Hence, these data indicate that visfatin can ameliorate immune stress injury in weaned piglets by exerting anti-inflammatory and antioxidant effects, enhancing immune organ and intestinal function.