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Nutrition and Health Program, Wageningen Center for Food Sciences/NIZO Food Research, 6710 BA Ede, The Netherlands
Nutrition and Health Program, Wageningen Center for Food Sciences, Wageningen, The Netherlands
* To whom correspondence should be addressed. E-mail: ingeborg.bovee{at}nizo.nl.
Dear Editor,
In our article published in January, 2006 in The Journal of Nutrition, we speculated that the increased mucin excretion that we observed in humans after consumption of rapidly fermentable fructo-oligosaccharides (FOS) was caused by the rapid production of organic acids from these oligosaccharides. Moreover, in our opinion, this mucin secretion likely reflects irritation and impairment of the intestinal barrier, as we observed in our earlier animal studies (1–4). In those animal studies, diet supplementation with rapidly fermentable fructo-oligosaccharides resulted in a doubling of mucin secretion, along with impaired intestinal barrier function, as indicated by increased translocation of salmonella through the gut wall to extra-intestinal organs like the liver and spleen. Thus, in our opinion, the stimulated mucin secretion indicates the need for the epithelial layer to protect itself against harmful substances.
However, according to Dr. Guarner, our assumption that mucin secretion reflects mucosal irritation is incorrect and not based on scientific evidence, because fiber and other indigestible substrates by themselves could also increase mucin secretion. Indeed, we demonstrated earlier (1–4) that several rapidly fermentable fibers (lactulose, FOS, and inulin) induce mucin secretion in rats. However, slowly fermentable or nonfermentable fibers like resistant starch, wheat fiber, and cellulose did not increase mucin secretion in our studies, nor did they increase salmonella translocation. This is in agreement with the references cited by Dr. Guarner, which also show increased mucin secretion by certain dietary fibers. However, and contrary to Dr. Guarner's statement, the cited references related to intestinal barrier function (Smidt-Wittig et al. and Strugala et al.) do not contain experimental data showing actual improvement of intestinal barrier function upon stimulation of mucin secretion by fiber supplementation, but only present speculations by the authors. In addition, mucin secretion and the subsequent increased salmonella translocation induced by rapidly fermentable fibers are virtually absent when diets are supplemented with calcium phosphate (100 mmol/kg), which increases luminal buffering capacity (2). Thus, in our studies, mucin secretion is associated with the rapid production of fermentation metabolites, such as lactic acid, in colonic contents with a low buffering capacity and not with mechanical stimulation by the presence of fiber itself.
Numerous articles (5–12) show that mucin excretion is enhanced by toxic or irritating components. We are not aware of papers showing that luminal substances considered nontoxic or nonharmful increase mucin secretion as well. According to Dr. Guarner, lactobacilli and epidermal growth factor induce mucin secretion although they are not considered irritants. These results with lactobacilli were found in in-vitro studies that do not neccesarily reflect the in-vivo situation. We observed in rats that the fructo-oligosaccharide-induced growth of lactic acid bacteria did not increase mucin secretion, provided that the diet was high in calcium (2). Epidermal growth factor indeed increases surface hydrophobicity and can subsequently protect against dextran sulfate sodium (DSS)-induced mucosal damage, but surface hydrophobicity is not a direct reflection of mucin secretion. We do not dispute that increased mucin secretion itself can protect against external mucosal damage. However, in our opinion, the stimulated mucin secretion in our studies indicates a need for the epithelial layer to protect itself against harmful substances.
Manuscript received 30 May 2006.
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LITERATURE CITED |
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 TOP LITERATURE CITED |
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1. Ten Bruggencate SJ, Bovee-Oudenhoven IM, Lettink-Wissink ML, Van der Meer R. Dietary fructooligosaccharides increase intestinal permeability in rats. J Nutr. 2005;135:837–42.
2. Ten Bruggencate SJ, Bovee-Oudenhoven IM, Lettink-Wissink ML, Katan MB, Van Der Meer R. Dietary fructo-oligosaccharides and inulin decrease resistance of rats to salmonella: protective role of calcium. Gut. 2004;53:530–5.
3. Ten Bruggencate SJ, Bovee-Oudenhoven IM, Lettink-Wissink ML, Van der Meer R. Dietary fructo-oligosaccharides dose-dependently increase translocation of salmonella in rats. J Nutr. 2003;133:2313–8.
4. Bovee-Oudenhoven IM, ten Bruggencate SJ, Lettink-Wissink ML, van der Meer R. Dietary fructo-oligosaccharides and lactulose inhibit intestinal colonisation but stimulate translocation of salmonella in rats. Gut. 2003;52:1572–8.
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6. Arnold JW, Klimpel GR, Niesel DW. Tumor necrosis factor (TNF alpha) regulates intestinal mucus production during salmonellosis. Cell Immunol. 1993;151:336–44.[Medline]
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8. Leiper K, Campbell BJ, Jenkinson MD, Milton J, Yu LG, Democratis J, Rhodes JM. Interaction between bacterial peptides, neutrophils and goblet cells: a possible mechanism for neutrophil recruitment and goblet cell depletion in colitis. Clin Sci (Lond). 2001;101:395–402.[Medline]
9. Moore BA, Sharkey KA, Mantle M. Neural mediation of cholera toxin-induced mucin secretion in the rat small intestine. Am J Physiol. 1993;265:G1050–6.[Medline]
10. Klinkspoor JH, Kuver R, Savard CE, Oda D, Azzouz H, Tytgat GN, Groen AK, Lee SP. Model bile and bile salts accelerate mucin secretion by cultured dog gallbladder epithelial cells. Gastroenterology. 1995;109:264–74.[Medline]
11. Shekels LL, Lyftogt CT, Ho SB. Bile acid-induced alterations of mucin production in differentiated human colon cancer cell lines. Int J Biochem Cell Biol. 1996;28:193–201.[Medline]
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