Psychosine Alleviates Colitis via Inhibiting Th1 and Th17 Cell Immune Responses in Inflammatory Bowel Diseases

Aberrant T-helper 1 (Th1) and Th17 cell activation is involved in the pathogenesis of inflammatory bowel disease (IBD). Psychosine is known to induce apoptosis, promote astrocyte activation, and inhibit osteoclastogenesis. However, the role of psychosine on Th1 and Th17 cell immune responses has not been previously reported. In this study, we investigate the role of psychosine in the modulation of CD4⁺ T cells.

Peripheral blood CD4⁺ (PB-CD4⁺) T cells were isolated from both IBD patients and healthy controls and cultured with psychosine, and the expression of IFN-γ and IL-17A was analyzed using a flow cytometer and enzyme-linked immunosorbent assay. The DSS-induced colitis model was established in mice; the expression of inflammatory cytokines was determined by flow cytometer and quantitative real-time polymerase chain reaction.

We found that psychosine suppresses the expression of IFN-γ and IL-17A and Th1 and Th17 cell differentiation in PB-CD4⁺ T cells. Meanwhile, psychosine was observed to inhibit the proliferation of PB-CD4⁺ T cells and intestinal mucosal inflammation. In vivo, psychosine alleviated DSS-induced colitis in mice by inhibiting Th1 and Th17 cell immune responses.

Our data reveal that psychosine reduces mucosal inflammation by preventing excessive Th1 and Th17 cell-mediated immune responses. Supplementation of psychosine may serve as a novel therapeutic approach for the treatment of IBD.