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Am J Physiol Regul Integr Comp Physiol 293: R1169-R1179, 2007. First published July 18, 2007; doi:10.1152/ajpregu.00770.2006
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INFLAMMATION AND CYTOKINES

Probiotics potentiate IL-6 production in IL-1beta-treated Caco-2 cells through a heat shock-dependent mechanism

Natasha Reilly,1 Vitaliy Poylin,1 Michael Menconi,1 Andrew Onderdonk,2 Stig Bengmark,3 and Per-Olof Hasselgren1

1Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts; 2Department of Pathology, Brigham Women's Hospital, Harvard Medical School, Boston, Massachusetts; and 3Liver Institute, University College, London University, United Kingdom

Submitted 5 November 2006 ; accepted in final form 13 July 2007

IL-6 may exert anti-inflammatory and protective effects in intestinal mucosa and enterocytes. The influence of probiotics on mucosal and enterocyte IL-6 production is not known. We tested the hypothesis that the probiotic bacteria Lactobacillus paracasei and Lactobacillus plantarum regulate IL-6 production in intestinal epithelial cells. Cultured Caco-2 cells were treated with 1 ng/ml of IL-1beta in the absence or presence of different concentrations of L. paracasei or L. plantarum followed by measurement of IL-6 production. The role of heat shock response was examined by determining the expression of heat shock protein 70 (hsp70) and hsp27, by downregulating their expression with small interfering RNA (siRNA), or by treating cells with quercetin. Treatment of the Caco-2 cells with IL-1beta resulted in increased IL-6 production, confirming previous reports from this laboratory. Probiotics alone did not influence IL-6 production, but the addition of probitoics to IL-1beta-treated cells resulted in a substantial augmentation of IL-6 production. Treatment of the Caco-2 cells with live L. paracasei increased cellular levels of hsp70 and hsp27 and the potentiating effect on IL-6 production was inhibited by quercetin and by hsp70 or hsp27 siRNA. Results suggest that probiotics may enhance IL-6 production in enterocytes subjected to an inflammatory stimulus and that this effect may, at least in part, be heat shock dependent.

intestine; inflammation; cytokines



Address for reprint requests and other correspondence: Address for correspondence: P.-O. Hasselgren, Dept. of Surgery, Beth Israel Deaconess Medical Center, 330 Brookline Ave., ST919, Boston, MA 02215 (e-mail: phasselg{at}bidmc.harvard.edu)




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