Study summary · research use only
Vasoactive intestinal peptide stabilizes intestinal immune homeostasis through maintaining interleukin-10 expression in regulatory B cells
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study used peripheral blood samples from patients with ulcerative colitis (UC) and healthy controls, along with a murine colitis model, to examine the role of vasoactive intestinal peptide (VIP) in regulatory B cell (Breg) function. Serum IL-10 and VIP levels were lower in IgE-positive (≥0.35 IU/mL) UC patients than in healthy controls, and Bregs isolated from these patients showed impaired immune suppressive function. IL-10 mRNA decayed spontaneously in Bregs, and this decay was reversed by VIP in culture; VIP also blocked binding of Tristetraprolin (TTP) to IL-10 mRNA that otherwise speeds its decay. Administration of VIP was associated with inhibition of experimental colitis in the mouse model.
Abstract
Rationale: Immune dysfunction is thought to play an important role in the pathogenesis of inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD). However, the underlying mechanism requires further investigation. Vasoactive intestinal peptide (VIP) has immune regulatory functions, but its role in immune regulatory activities in the intestinal mucosa is not fully understood. This study aims to elucidate the role of VIP in the regulation of regulatory B cell (Breg) function in the intestine. Methods: Peripheral blood samples were collected from UC patients and healthy control (HC) subjects. Bregs were isolated from these samples and their immune regulatory function was analyzed. A murine colitis model was established to test the role of VIP in inhibiting inflammation in the intestine. Results: Serum IL-10 and VIP levels were lower in IgE+ (≥0.35 IU/mL) UC patients than that in HC subjects. The immune suppressive function of Bregs isolated from IgE+ UC patients was impaired. IL-10 mRNA decayed spontaneously in Bregs, which was reversed by VIP added to the culture. Tristetraprolin (TTP) bound IL-10 mRNA to speed its decay, which was blocked by VIP in the culture. Administration of VIP efficiently inhibited experimental colitis. Conclusions: Insufficient VIP levels in the microenvironment speeds IL-10 mRNA decay to cause Breg dysfunction. Administration of VIP can inhibit experimental colitis, suggesting the translational potential of VIP in the treatment of IgE+ UC.
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