Bifidobacterium infantis Induces Protective Colonic PD-L1 and Foxp3 Regulatory T Cells in an Acute Murine Experimental Model of Inflammatory Bowel Disease

摘要

Background/Aims The current study aims to investigate the protective effects of Bifidobacterium infantis on the abnormal immune response to inflammatory bowel disease (IBD) in dextran sodium sulfate (DSS)-induced colitis. Methods Eight-week-old BALB/c mice were separated into five groups at random (control, DSS, DSS+B9 [ B . infantis 1×10 ~(9) CFU], DSS+B8 [ B . infantis 1×10 ~(8) CFU], and DSS+B7 [ B . infantis 1×10 ~(7) CFU]). Colitis was induced by 5% DSS ad libitum for 7 days, at which time we assessed weight, the disease activity index (DAI) score, and the histological damage score. The nuclear transcription factor Foxp3 (a marker of Treg cells), cytokines interleukin-10 (IL-10) and transforming growth factor β1 (TGF-β1), and related proteins (programmed cell death ligand 1 [PD-L1] and programmed cell death 1 [PD-1]) were detected by an immunohistochemical method and Western blot. Results B . infantis increased weight, decreased DAI scores and histological damage scores, increased the protein expression of Foxp3 (p&0.05) and cytokines IL-10 and TGF-β1 in mouse colon tissue (p&0.05), and increased the expression of PD-L1 in the treatment groups relative to that in the DSS group (p&0.05). The effect of B . infantis on Foxp3 and PD-L1 was dose dependent in the treatment groups (p&0.05). PD-L1 was positively correlated with Foxp3, IL-10, and TGF-β1. Conclusions In a mouse model of IBD, B . infantis can alleviate intestinal epithelial injury and maintain intestinal immune tolerance and thus may have potential therapeutic value for the treatment of immune damage in IBD.