Commentary: associations between immune activation, intestinal permeability and irritable bowel syndrome.

None required in se rm -0 07 71 44 0, v er si on 1 8 Ja n 20 13 We thank Dr. Jovani and colleagues for their comments regarding our review on associations between irritable bowel syndrome (IBS) and gut inflammation. Many studies have assessed inflammatory markersin IBS and yielded a considerable amount ofheterogeneous data, which made the link between IBS and inflammation difficult to evaluate. Thus, the aim of our review was to clarify this link by determining if the levels of inflammatory markers in fecal samples, blood samples or intestinal biopsies were higher in IBS patients than in healthy controls. Other risk factors such as stress and psychological factors are involved in IBS etiology1, however these were not described in detail since this was out of the scope of the present review. We also fully agree that alteration of the gut microflora can contribute to IBS etiopathogenesis.Actually, dysbiosis was quite consistently reported in IBS.2Small intestinal bacterial overgrowth (SIBO) has been somewhat associated with IBS3although the existence of acausal link between IBS and SIBO is still under debate because most of the existing studies are methodologically biased or lack the appropriate controls.4 In line with a possible involvement of dysbiosis and/or SIBO in IBS, recent studies have shown beneficial effects of the antibiotics mesalazineand rifaximin on symptomatology.5Probiotics can relieve symptoms in some cases as well.6Nevertheless, large randomized and controlled trials are still needed to further evaluate the effectiveness of anti-inflammatory agents and probiotics for treating IBS.Associations between beneficial effects of antibiotics and presence of SIBO are lackingas well.2 Despite these shortcomings, modulation of the intestinal flora could indeed be a prosperous direction of future research. The pathophysiological in se rm -0 07 71 44 0, v er si on 1 8 Ja n 20 13 consequences of these microflora changes in IBS are not well understood.However, one explanation could be the increase in intestinal permeability following alteration of tight junction complexes in intestinal epithelial cells and subsequent immune activation within the mucosa.7 Acknowledgement: The authors' declarations of personal and financial interests areunchanged from those in the original article.8 References1. Chang L. The role of stress on physiologic responses and clinical symptoms inirritable bowel syndrome. Gastroenterology 2011;140(3):761-5.2. Dahlqvist G, Piessevaux H. Irritable bowel syndrome: the role of the intestinalmicrobiota, pathogenesis and therapeutic targets. Acta Gastroenterol Belg2011;74(3):375-80.3. Ford AC, Spiegel BM, Talley NJ, Moayyedi P. Small intestinal bacterialovergrowth in irritable bowel syndrome: systematic review and meta-analysis. ClinGastroenterol Hepatol 2009;7(12):1279-86.4. Spiegel BM. Questioning the bacterial overgrowth hypothesis of irritablebowel syndrome: an epidemiologic and evolutionary perspective. Clin GastroenterolHepatol 2011;9(6):461-9; quiz e59.5. Sachdev AH, Pimentel M. Antibiotics for irritable bowel syndrome: rationaleand current evidence. Curr Gastroenterol Rep 2012;14(5):439-45.6. Clarke G, Cryan JF, Dinan TG, Quigley EM. Review article: probiotics for thetreatment of irritable bowel syndrome--focus on lactic acid bacteria. AlimentPharmacol Ther 2012;35(4):403-13.7. Ulluwishewa D, Anderson RC, McNabb WC, Moughan PJ, Wells JM, Roy NC.Regulation of tight junction permeability by intestinal bacteria and dietarycomponents. J Nutr 2011;141(5):769-76.8. Matricon J, Meleine M, Gelot A, et al. Review article: associations betweenimmune activation, intestinal permeability and the irritable bowel syndrome.Aliment Pharmacol Ther 2012.inserm-00771440,version1-8Jan2013