Capsaicin, the main active component of chili peppers, binds via the receptor for vallinoid 1, expressed by neurons as well as a variety of immunocytes. In Mucosal Immunology, Basu and colleagues use two different mouse models of type 1 diabetes to investigate whether this widely consumed compound modulates immune responses. The administration of capsaicin orally results in a lower incidence of both spontaneous and induced type 1 diabetes, but capsaicin administration via other routes does not. Immune responses are diminished in the pancreatic lymph nodes—considered part of the gut-associated lymphoid tissue—but are unaffected systemically. The protective effects depend on a gut macrophage population with enhanced expression of the immunomodulatory molecule IL-10. Furthermore, bone marrow chimeras combined with deletion of the receptor for vallinoid 1 demonstrate that the expression of this receptor on macrophages is essential for capsaicin's immunomodulatory effects. This study demonstrates mechanistically how a common food component can modulate autoimmune responsiveness.

Mucosal Immunol. 5, 76–86 (2012)