LETTER TO THE EDITOR
Food and intestinal barrier function in irritable bowel syndrome
Article first published online: 22 AUG 2012
© 2012 Blackwell Publishing Ltd
Neurogastroenterology & Motility
Volume 24, Issue 9, page 888, September 2012
How to Cite
Matuchansky, C. (2012), Food and intestinal barrier function in irritable bowel syndrome. Neurogastroenterology & Motility, 24: 888. doi: 10.1111/j.1365-2982.2012.01978.x
- Issue published online: 22 AUG 2012
- Article first published online: 22 AUG 2012
I read with great interest the review by Camilleri et al.1 on intestinal barrier function. After a clear analysis of basic physiology, measurement and potential neuroimmune and bacterial modulation of permeability, they retained three lines of evidence that support a link between abnormal intestinal permeability and functional gastrointestinal (GI) disorders, especially irritable bowel syndrome (IBS), i.e., infection, genetic predisposition, and stress. I have a main concern about this comprehensive review: the authors omitted to discuss the potentially central role of food, a factor yet recently reported as often forgotten in IBS.2
Indeed, besides stimulation of mechano- or chemoreceptors, activation of motor reflexes pathways, GI hormone release and luminal fluid secretion, dietary food can act on intestinal barrier function through several immune-neuroimmune mechanisms : (i) first, true food allergy or sensitization, which affects 4–8% of children and 3–4% of adults in westernized countries2; breakdown of oral immune tolerance leads to recruitment of mucosal mast cells (MCs); MCs and their secreted mediators alter intestinal permeability via different proinflammatory pathways, IgE-CD23-mediated mucosal transport playing an amplification role; while 20–67% of IBS individuals complain of subjective food intolerance or aversion, and 50–90% of presumed food allergies are not actually allergies, atopic IBS was suggested as a new objective IBS subgroup2; (ii) second, luminal nutrients, such as glucose and fatty acids, may stimulate enterochromaffin cells (ECCs) with resulting secretion of serotonin and signaling peptides which act as paracrine signal transducers to the enteric nervous system (ENC); there is evidence for ENC communication with the mucosal immune system, and also for epithelial cells – enteric bacteria communication via the luminal release from ECCs of molecules that can modulate microbial activity3 and thereby intestinal permeability; (iii) third, some nutrients, including poorly absorbable components, may induce changes in colonic commensal flora, fermentation of luminal contents, and permeability; (iv) finally, after degradation in the upper GI tract, food material, such as haptens and polypeptides, may pass directly by paracellular diffusion through high-capacity pore pathway in the tight junctions, while larger macromolecules may pass through low-capacity leak pathway, and larger molecular complexes across enterocytes by transcytosis4; without inducing true allergy, these antigen passages may result, in predisposed individuals and as well in conventional as in postinfectious IBS,5 in infraclinical inflammation in distal ileum and colon and in altered intestinal permeability.
Conflict of Interest
The author has declared no conflict of interest.