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Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 BMC+Microbiol 2015 ; 15 (ä): ä Nephropedia Template TP
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Lactobacillus acidophilus attenuates Salmonella-induced intestinal inflammation via TGF-? signaling #MMPMID26446848
Huang IF; Lin IC; Liu PF; Cheng MF; Liu YC; Hsieh YD; Chen JJ; Chen CL; Chang HW; Shu CW
BMC Microbiol 2015[]; 15 (ä): ä PMID26446848show ga
Background: Salmonella is a common intestinal pathogen that causes acute and chronic inflammatory response. Probiotics reduce inflammatory cytokine production and serve as beneficial commensal microorganisms in the human gastrointestinal tract. TGF-? (transforming growth factor ?)/SMAD and NF-?B signaling play important roles in inflammation in intestinal cells. However, the involvement of the signaling in regulating inflammation between Salmonella and probiotics is not fully understood. Methods: L. acidophilus and prebiotic inulin were used to treat human intestinal Caco-2 cells prior to infection with Salmonella. The cells were harvested to examine the cytokines and MIR21 expression with immunoblotting and real-time PCR. NF-?B and SMAD3/4 reporter vectors were transfected into cells to monitor inflammation and TGF-?1 signaling, respectively. Results: In this study, we showed that the probiotic L. acidophilus decreased Salmonella-induced NF-?B activation in human intestinal Caco-2 cells. Expression of the inflammatory cytokines, TNF-? and IL-8, in L. acidophilus-pretreated cells was also significantly lower than that in cells infected with Salmonella alone. Moreover, TGF-?1 and MIR21 expression was elevated in cells pretreated with L. acidophilus or synbiotic, a combination of inulin and L. acidophilus, compared to that in untreated cells or cells infected with S. typhimurium alone. By contrast, expression of SMAD7, a target of MIR21, was accordingly reduced in cells treated with L. acidophilus or synbiotics. Consistent with TGF-?1/MIR21 and SMAD7 expression, SMAD3/4 transcriptional activity was significantly higher in the cells treated with L. acidophilus or synbiotics. Furthermore, TGF-?1 antibody antagonized the SMAD3/4 and NF-?B transcriptional activity modulated by L. acidophilus in intestinal cells. Conclusion: Our results suggest that the TGF-?1/MIR21 signaling pathway may be involved in the suppressive effects of L. acidophilus on inflammation caused by S. typhimurium in intestinal Caco-2 cells. Electronic supplementary material: The online version of this article (doi:10.1186/s12866-015-0546-x) contains supplementary material, which is available to authorized users.