Inhibiting the proinflammatory cytokine tumor necrosis factor dramatically reduces gut inflammation and largely restores the gut barrier in Crohn's disease. Our data confirm the central role of TNF in gut barrier modulation in inflammatory conditions in vivo.

ASCA is strongly associated with familial CD in Belgium, and 21% of healthy family members also display the marker. The association is much weaker in patients belonging to mixed families. ASCA is a stable marker and is not a secondary phenomenon due to increased intestinal permeability.

Short-term exposure to nicotine does not alter normal basal or NSAID-induced gut barrier function or transit. 51Cr-EDTA and the respective sugar markers correlate well in in vivo permeability testing in healthy humans. The radioactive test detects more NSAID-induced permeability increase than does the lactulose/mannitol ratio permeability test.

Background: Smoking modulates inflammatory bowel disease, protecting from ulcerative colitis on the one hand and worsening the course of Crohn’s disease on the other. This influence might occur through changes in intestinal permeability, because permeability is increased in most patients with Crohn’s disease. Aim: To study the influence of smoking on small intestinal permeability and its increase induced by indomethacin. Methods: 50 smokers and 50 nonsmokers underwent a 51Cr‐EDTA basal permeability test and the same test after challenge with indomethacin 125 mg p.o. Results: Small intestinal permeability was the same in smokers (median 1.22%; IQR 1.00–1.58) and nonsmokers (1.24%; 0.94–1.66). Basal small intestinal permeability was lower in females (1.09%; 0.87–1.33) than in males (1.48%; 1.18–1.88). Indomethacin challenge increased permeability by 110% (71–141) in smokers, vs. 156% (78–220) in the nonsmokers (P=0.04). Conclusion: Smoking reduces the effect of NSAID on small intestinal permeability. It is therefore unlikely that the adverse effect of smoking on Crohn’s disease is related to its influence on intestinal permeability.

SUMMARY BackgroundButyrate, a colonic metabolite of carbohydrates, is considered as the major energy source for the colonic mucosa. An impaired butyrate metabolism has been reported in ulcerative colitis (UC), however, the cause still remains unknown.