Summary Background : Butyrate exerts anti‐inflammatory effects in experimental colitis and on Crohn's disease lamina propria mononuclear cells in vitro. Aim : To explore the efficacy and safety of oral butyrate in Crohn's disease. Methods : Thirteen patients with mild–moderate ileocolonic Crohn's disease received 4 g/day butyrate as enteric‐coated tablets for 8 weeks. Full colonoscopy and ileoscopy were performed before and after treatment. Endoscopical and histological score, laboratory data, Crohn's disease activity index and mucosal interleukin (IL)‐1β, IL‐6, IL‐12, interferon‐γ, tumour necrosis factor‐α and nuclear factor‐kappa B (NF‐κB) were assessed before and after treatment. Results : One patient withdrew from the study, and three patients did not experience clinical improvement. Among the nine patients (69%) who responded to treatment, seven (53%) achieved remission and two had a partial response. Endoscopical and histological score significantly improved after treatment at ileocaecal level (P < 0.05). Leucocyte blood count, erythrocyte sedimentation rate and mucosal levels of NF‐κB and IL‐1β significantly decreased after treatment (P < 0.05). Conclusions : Oral butyrate is safe and well tolerated, and may be effective in inducing clinical improvement/remission in Crohn's disease. These data indicate the need for a large investigation to extend the present findings, and suggest that butyrate may exert its action through downregulation of NF‐κB and IL‐1β.

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Enterocyte apoptosis is increased in involved areas of Crohn's disease. This increase is not mediated by a Fas-Fas ligand mechanism or by an abnormal E-cadherin distribution. Increased matrix metalloproteinase-1 release from lamina propria mononuclear cells might be one of the possible mechanisms responsible for the increased enterocyte apoptosis in Crohn's disease.

Our findings show that peripheral IgM memory B cells are reduced in inflammatory bowel disease patients and this defect seems to be related to the impairment of splenic function.