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10.1186/s40168-018-0433-4 http://scihub22266oqcxt.onion/10.1186/s40168-018-0433-4 C5865374!5865374!29566748     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29566748&cmd=llinks): Failed to open stream: HTTP request failed! 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High salt diet exacerbates colitis in mice by decreasing Lactobacillus levels and butyrate production |pdf=|usr=}}{{29566748}} gab.com Text High salt diet exacerbates colitis in mice by decreasing Lactobacillus levels and butyrate production JO: Microbiome http://www.kidney.de/pget.php?&tw=1&pmid=29566748 #FOAvip Background: Changes in hygiene and dietary habits, including increased consumption of foods high in fat, simple sugars, and salt that are known to impact the composition and function of the intestinal microbiota, may explain the increase in prevalence of chronic inflammatory diseases. High salt consumption has been shown to worsen autoimmune encephalomyelitis and colitis in mouse models through p38/MAPK signaling pathway. However, the effect of high salt diet (HSD) on gut microbiota and on intestinal immune homeostasis, and their roles in determining vulnerability to intestinal inflammatory stimuli are unknown. Here, we investigate the role of gut microbiota alterations induced by HSD on the severity of murine experimental colitis. Results: Compared to control diet, HSD altered fecal microbiota composition and function, reducing Lactobacillus sp. relative abundance and butyrate production. Moreover, HSD affected the colonic, and to a lesser extent small intestine mucosal immunity by enhancing the expression of pro-inflammatory genes such as Rac1, Map2k1, Map2k6, Atf2, while suppressing many cytokine and chemokine genes, such as Ccl3, Ccl4, Cxcl2, Cxcr4, Ccr7. Conventionally raised mice fed with HSD developed more severe DSS- (dextran sodium sulfate) and DNBS- (dinitrobenzene sulfonic acid) induced colitis compared to mice on control diet, and this effect was absent in germ-free mice. Transfer experiments into germ-free mice indicated that the HSD-associated microbiota profile is critically dependent on continued exposure to dietary salt. Conclusions: Our results indicate that the exacerbation of colitis induced by HSD is associated with reduction in Lactobacillus sp. and protective short-chain fatty acid production, as well as changes in host immune status. We hypothesize that these changes alter gut immune homeostasis and lead to increased vulnerability to inflammatory insults. Electronic supplementary material: The online version of this article (10.1186/s40168-018-0433-4) contains supplementary material, which is available to authorized users. Twit Text FOAVip High salt diet exacerbates colitis in mice by decreasing Lactobacillus levels and butyrate production ????Microbiome http://www.kidney.de/pget.php?&tw=1&pmid=29566748 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29566748 #FOAvip English Wikipedia <ref>{{Cite pmid|29566748}}</ref> High salt diet exacerbates colitis in mice by decreasing Lactobacillus levels and butyrate production #MMPMID29566748 Miranda PM; De Palma G; Serkis V; Lu J; Louis-Auguste MP; McCarville JL; Verdu EF; Collins SM; Bercik P Microbiome 2018[]; 6 (ä): ä PMID29566748show ga Background: Changes in hygiene and dietary habits, including increased consumption of foods high in fat, simple sugars, and salt that are known to impact the composition and function of the intestinal microbiota, may explain the increase in prevalence of chronic inflammatory diseases. High salt consumption has been shown to worsen autoimmune encephalomyelitis and colitis in mouse models through p38/MAPK signaling pathway. However, the effect of high salt diet (HSD) on gut microbiota and on intestinal immune homeostasis, and their roles in determining vulnerability to intestinal inflammatory stimuli are unknown. Here, we investigate the role of gut microbiota alterations induced by HSD on the severity of murine experimental colitis. Results: Compared to control diet, HSD altered fecal microbiota composition and function, reducing Lactobacillus sp. relative abundance and butyrate production. Moreover, HSD affected the colonic, and to a lesser extent small intestine mucosal immunity by enhancing the expression of pro-inflammatory genes such as Rac1, Map2k1, Map2k6, Atf2, while suppressing many cytokine and chemokine genes, such as Ccl3, Ccl4, Cxcl2, Cxcr4, Ccr7. Conventionally raised mice fed with HSD developed more severe DSS- (dextran sodium sulfate) and DNBS- (dinitrobenzene sulfonic acid) induced colitis compared to mice on control diet, and this effect was absent in germ-free mice. Transfer experiments into germ-free mice indicated that the HSD-associated microbiota profile is critically dependent on continued exposure to dietary salt. Conclusions: Our results indicate that the exacerbation of colitis induced by HSD is associated with reduction in Lactobacillus sp. and protective short-chain fatty acid production, as well as changes in host immune status. We hypothesize that these changes alter gut immune homeostasis and lead to increased vulnerability to inflammatory insults. Electronic supplementary material: The online version of this article (10.1186/s40168-018-0433-4) contains supplementary material, which is available to authorized users. äHigh salt diet exacerbates colitis in mice by decreasing Lactobacillus(epmc).pdf DeepDyve Pubget Overpricing