Sodium Alginate Modulates Immunity, Intestinal Mucosal Barrier Function, and Gut Microbiota in Cyclophosphamide-Induced Immunosuppressed BALB/c Mice

This study investigated the protective effects of sodium alginate (SA) on the gut microbiota, immunity, and intestinal mucosal barrier function in cyclophosphamide-induced immunosuppressed BALB/c mice. SA alleviated spleen tissue damage and restored impaired immune functions, such as increasing the immune organ index, decreasing splenic T lymphocytes, and markedly increasing the secretion of serum immunoglobulins and cytokines in immunosuppressed mice. In addition, SA reversed the intestinal mucosal injury and increased the intestinal permeability by upregulating the expression of tight junction proteins. Moreover, SA decreased gut inflammation by reducing serum D-lactic acid (D-LA) and lipopolysaccharide (LPS) concentrations and downregulating toll-like receptor 4 (Tlr4) and mitogen-activated protein kinase (Mapk) pathway expression. Furthermore, SA significantly increased the abundance of beneficial bacteria (Lactobacillus, Roseburia, and Lachnospiraceae NK4A136) and decreased pathogenic bacteria (Helicobacter, Peptococcus, and Tyzzerella) in the intestine as determined by 16S rRNA gene high-throughput sequencing. In conclusion, our study provides a scientific basis for SA as a functional food in modulating gut microbiota and protecting against intestinal mucosal injury and indicates that SA has potential application for enhancing immunity.

Automated summary

This study investigated the protective effects of sodium alginate on gut microbiota, immunity, and intestinal mucosal barrier function in immunosuppressed mice. The results showed that SA alleviated spleen tissue damage, restored impaired immune functions, reversed intestinal mucosal injury, and modulated gut microbiota by increasing beneficial bacteria and decreasing pathogenic bacteria in the intestine. The study suggests that SA has the potential to enhance immunity and protect against intestinal mucosal injury.