The paper by Philippe and colleagues¹ in this issue of Gut provides new insight into the pathophysiology of inflammatory bowel disease (IBD) (see page 815). It also offers a new line of potential therapy for these diseases. The paper demonstrates the upregulation of μ opioid receptors (MOR) in inflamed tissue from patients with Crohn’s disease and ulcerative colitis, and localises the upregulation, at least in part, to lamina propria mononuclear cells, including CD4+ and CD8+ lymphocytes. The paper also shows that a MOR agonist DALDA reduced the secretion of the important proinflammatory cytokine tumour necrosis factor α (TNF-α) from colonic tissue from IBD and control subjects. The study was a logical extension of previous work by the same authors showing that the MOR agonist DALDA reduced inflammation in two murine models of experimental colitis and that mice genetically deficient in the MOR were highly susceptible to induction of inflammation in the gut.² Taken together, these findings not only demonstrate the therapeutic potential of drugs that target the MOR in IBD, but also that endogenous opiate may confer a measure of protection against inflammation. …