Effects of Lactobacillus casei NCU011054 on immune response and gut microbiota of cyclophosphamide induced immunosuppression mice

Lactobacillus (L.) casei NCU011054 isolated from infant feces has been proven to be a potential probiotic in vitro. The present study aimed to investigate the effects of L. casei NCU011054 on the immune response and gut microbiota in cyclophosphamide (CP)-induced immunosuppression mice. Results indicated that L. casei NCU011054 could increase the levels of mucin (Muc2) and tight junction proteins (ZO-1, occludin and claudin-1). Moreover, L. casei NCU011054 was found to upregulate TLRs/NF-kappa B pathway (TLR-2, TLR-4, TLR-6, p65 and NF-kappa B) and two transcription factors (T-bet and GATA-3) mRNA levels, and enhance the number of CD4+T cells. Th1-related cytokines (IL-12p70, IFN-gamma and TNF-alpha) and Th2-related cytokines (IL-2, IL-4, IL-6 and IL-10) significantly increased after L. casei NCU011054 treatment. More importantly, L. casei NCU011054 increased the ratio of T-bet to GATA-3 and IFN-gamma to IL-4. Apart from these, L. casei NCU011054 remodeled gut microbiota and modulated gut metabolites in CP-induced immunosuppressed mice. The correlation analysis showed that Lactobacillus upregulated by L. casei NCU011054 was positively correlated with TLRs/NF-kappa B pathway, and the ratio of T-bet to GATA-3 and IFN-gamma to IL-4. All findings revealed that L. casei NCU011054 could improve in-testinal immune dysfunction and modulate Th1/Th2 balance via TLRs/NF-kappa B pathway in CP-induced immu-nosuppressed mice.

Automated summary

L. casei NCU011054 was found to improve intestinal immune dysfunction and modulate Th1/Th2 balance via the TLRs/NF-kappa B pathway in cyclophosphamide-induced immunosuppressed mice. It increased the levels of mucin and tight junction proteins, upregulated TLRs/NF-kappa B pathway and two transcription factors, and enhanced CD4+T cell numbers. It also increased Th1- and Th2-related cytokines and remodeled gut microbiota and gut metabolites.