The immunomodulatory effects of Bifidobacterium lactis XLTG11 on cyclophosphamide-induced immune dysfunction in mice.
TL;DR
Findings demonstrate that B. lactis XLTG11 can modulate immune function, and the underlying mechanisms involve repairing the intestinal mucosal barrier, regulating the levels of immune cells and cytokines, and maintaining gut microbiota homeostasis.
Abstract
Previous studies have demonstrated that Bifidobacterium lactis (B. lactis) XLTG11 exerts significant immunomodulatory effects. However, the underlying mechanisms remain unclear. To investigate these mechanisms, BALB/c mice were randomly divided into three groups: normal control (NC), model control (MC), and B. lactis XLTG11 (XL) groups. We assessed spleen and thymus indices, jejunal histopathology, leukocyte and IgA cell counts, as well as the levels of interferon (IFN)-γ, interleukin (IL)-2, IL-4, IL-12, and secretory IgA (SIgA) in the small intestine. We also analysed the composition and diversity of the gut microbiota. The results showed that B. lactis XLTG11 restored villus height and crypt depth, thereby alleviating jejunal tissue damage. Furthermore, B. lactis XLTG11 treatment significantly increased the counts of leukocytes, goblet cells, and IgA cells, and elevated the levels of the aforementioned cytokines and SIgA. It also increased thymus indices without affecting spleen indices. Regarding the gut microbiota, B. lactis XLTG11 reduced the Bacillota/Bacteroidota ratio and modulated microbial composition and diversity. Spearman's correlation analysis revealed significant associations between specific microbial taxa and the immune parameters measured above. Collectively, these findings demonstrate that B. lactis XLTG11 can modulate immune function, and the underlying mechanisms involve repairing the intestinal mucosal barrier, regulating the levels of immune cells and cytokines, and maintaining gut microbiota homeostasis.