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We read with interest the article by Garcia-Lafuente et al (Gut 2001;48:503–7). Their results demonstrate that strains of endemic gut bacteria can affect gut mucosal barrier function, as measured by intestinal permeability, and that the effect may be potentially beneficial or harmful depending on the specific bacterial strains administered.
These findings help to explain and corroborate the interesting findings that have been emerging from clinical and experimental studies investigating the use of probiotics in inflammatory bowel disease (IBD). It is known that development of colonic inflammation in genetic models of IBD is dependent on the presence of intestinal bacteria. In human studies, an imbalance in colonic bacteria has been described in patients with IBD with a reduction in potentially protective organisms such as bifidobacteria and lactobacilli and an increase in Escherichia coli. Furthermore, treatment with probiotics such as lactobacilli has been shown to reduce intestinal inflammation and inflammatory response in experimental models of colitis and to reduce symptoms and inflammatory scores in patients with IBD.
We have recently investigated the effect of Lactobacillus plantarum species 299 on the gut mucosal barrier both in patients with ulcerative colitis and in the interleukin 10 knockout mouse model of colitis.1, 2 This probiotic was found to improve gut mucosal barrier function in the mouse model, as measured by a reduction in gut permeability and a reduction in the concentration of circulating antibody to endotoxin. These changes correlated positively with a reduction in colonic inflammation. In a study of patients with ulcerative colitis, Lactobacillus plantarum probiotic therapy was also found to improve gut mucosal barrier function, as measured by a reduction in the circulating antibody to endotoxin.2 The findings of our studies and those of Garcia-Lafuente et al suggest that probiotics such as Lactobacillus plantarum are capable of improving gut mucosal barrier function in both normal and inflamed bowel. It is possible that this probiotic induced enhancement of the gut barrier may be a mechanism by which probiotics are effective in reducing intestinal inflammation in experimental models of colitis and IBD.
We value the comments made by Mr Kennedy et al and are grateful to them for bringing to our attention their report to the Surgical Research Society on the effect of Lactobacillus plantarum species 299 on the gut mucosal barrier in the interleukin 10 knockout model of colitis. While we agree with their points regarding the usefulness of some probiotic strains for the prevention of gut barrier dysfunction associated with mucosal inflammatory conditions, we also would like to stress the fact that bacteria may also influence colonic barrier function in a normal setting. In our experimental model, we were able to detect changes in the colonic permeability to a small molecular size probe induced by commensal bacteria, without any significant effect on the lumen to blood passage of a large molecular size probe—that is, excluding changes due to epithelial cell damage. This finding suggests that in a physiological state, colonic permeability can be influenced by the quality of the flora colonising the mucosal surfaces. Further studies are needed for a better understanding of the interplay between resident bacteria and the host at the mucosal interface.
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