Purpose of review: The relationship between allergy and motility has been controversial. There is, however, accumulating evidence demonstrating that mucosal allergic responses may disrupt gut motility, and may also potentially alter nociceptive pathways to cause visceral hyperalgesia.
Recent findings: Experimental studies implicate T helper 2 cells and the cytokines interleukin-4 and -13 in antigen-induced dysmotility, and interleukin-5 in the pathogenesis of mucosal eosinophilia. Both mast cells and eosinophils play obligatory roles in different forms of experimental antigen-induced dysmotility. Overall clinical findings appear to implicate eosinophil infiltration in proximal and distal dysmotility syndromes (oesophageal, gastric and colorectal), and induced mast cell degranulation in mid-gut dysmotility. There is also evidence that mucosal allergic responses may induce long-term changes in visceral perception, including alteration of limbic response, leading to sustained abnormality in visceral sensation.
Summary: Clinical evidence implicating mucosal allergic responses in dysmotility has been extended to include disorders considered previously entirely functional, such as in some cases of irritable bowel syndrome. Only a proportion of cases are, however, caused by food allergy and a future challenge is to differentiate patients with similar symptoms, but induced by different mechanisms.