Involvement of Intracellular Signaling in the IL-1[beta] Inhibitory Effect on Fructose Intestinal Absorption

A variety of bacteria and their excreted/secreted products having direct effects on epithelial ion transport and permeability and the release of cytokines during bacterial infection may impact directly on epithelial function. Interleukin-1[beta] (IL-1[beta]) is a pleiotropic cytokine that affects th...

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Published inJournal of cellular physiology Vol. 230; no. 4; p. 896
Main Authors Rodriguez-Yoldi, María J, Gascon, Sonia, Barranquero, Cristina, Garcia-Barrios, Alberto, Osada, Jesús
Format Journal Article
LanguageEnglish
Published Hoboken Wiley Subscription Services, Inc 01.04.2015
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Summary:A variety of bacteria and their excreted/secreted products having direct effects on epithelial ion transport and permeability and the release of cytokines during bacterial infection may impact directly on epithelial function. Interleukin-1[beta] (IL-1[beta]) is a pleiotropic cytokine that affects the intestinal absorption of nutrients. The aim of this work was to study the intracellular signaling pathways involved in the inhibitory effect of IL-1[beta] on D-fructose intestinal transport in rabbit jejunum and Caco-2 cells. The results show that the cytokine inhibitory effect was completely reversed in presence of proteasome or PKC selective inhibitors in IL-1[beta] treated rabbits. In addition, the activation of PI3K abolished the IL-1[beta] effect. Likewise, these results were confirmed in Caco-2 cells. In addition, p-PI3K expression was increased by IL-1[beta]-treatment whereas the expression of p-PKC[alpha] was not significantly affected. In summary, the results suggest that IL-1[beta] could regulate the activation of pPKC[alpha] 73, pPI3K 55, and NF-kB proteins. These events could exert an inhibitory effect on fructose intestinal absorption by a modification of GLUT5 insertion to brush-border membrane and/or the functional transporter activity. This effect is independent of hormonal milieu and nervous stimuli. J. Cell. Physiol. 230: 896-902, 2015. © 2014 Wiley Periodicals, Inc.
ISSN:0021-9541
1097-4652
DOI:10.1002/jcp.24820