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10.1016/j.chom.2016.03.004 http://scihub22266oqcxt.onion/10.1016/j.chom.2016.03.004 C4832419!4832419!27078066     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27078066&cmd=llinks): Failed to open stream: HTTP request failed! 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Depletion of butyrate-producing Clostridia from the gut microbiota drives an aerobic luminal expansion of Salmonella |pdf=|usr=}}{{27078066}} gab.com Text Depletion of butyrate-producing Clostridia from the gut microbiota drives an aerobic luminal expansion of Salmonella JO: Cell Host Microbe http://www.kidney.de/pget.php?&tw=1&pmid=27078066 #FOAvip The mammalian intestine is host to a microbial community that prevents pathogen expansion through unknown mechanisms, while antibiotic treatment can increase susceptibility to enteric pathogens. Here we show that streptomycin treatment depleted commensal, butyrate-producing Clostridia from the mouse intestinal lumen, leading to decreased butyrate levels, increased epithelial oxygenation and aerobic expansion of Salmonella enterica serovar Typhimurium. Epithelial hypoxia and Salmonella restriction could be restored by tributyrin treatment. Clostridia depletion and aerobic Salmonella expansion were also observed in the absence of streptomycin treatment in genetically resistant mice, but proceeded with slower kinetics and required the presence of functional Salmonella type III secretion systems. The Salmonella cytochrome bd-II oxidase synergized with nitrate reductases to drive luminal expansion, and both were required for fecal-oral transmission. We conclude that Salmonella virulence factors and antibiotic treatment promote pathogen expansion through the same mechanism: depletion of butyrate-producing Clostridia to elevate epithelial oxygenation, allowing aerobic Salmonella growth. Twit Text FOAVip Depletion of butyrate-producing Clostridia from the gut microbiota drives an aerobic luminal expansion of Salmonella ????Cell Host Microbe http://www.kidney.de/pget.php?&tw=1&pmid=27078066 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27078066 #FOAvip English Wikipedia <ref>{{Cite pmid|27078066}}</ref> Depletion of butyrate-producing Clostridia from the gut microbiota drives an aerobic luminal expansion of Salmonella #MMPMID27078066 Rivera-Chávez F; Zhang LF; Faber F; Lopez CA; Byndloss MX; Olsan EE; Xu G; Velazquez EM; Lebrilla CB; Winter SE; Bäumler AJ Cell Host Microbe 2016[Apr]; 19 (4): 443-54 PMID27078066show ga The mammalian intestine is host to a microbial community that prevents pathogen expansion through unknown mechanisms, while antibiotic treatment can increase susceptibility to enteric pathogens. Here we show that streptomycin treatment depleted commensal, butyrate-producing Clostridia from the mouse intestinal lumen, leading to decreased butyrate levels, increased epithelial oxygenation and aerobic expansion of Salmonella enterica serovar Typhimurium. Epithelial hypoxia and Salmonella restriction could be restored by tributyrin treatment. Clostridia depletion and aerobic Salmonella expansion were also observed in the absence of streptomycin treatment in genetically resistant mice, but proceeded with slower kinetics and required the presence of functional Salmonella type III secretion systems. The Salmonella cytochrome bd-II oxidase synergized with nitrate reductases to drive luminal expansion, and both were required for fecal-oral transmission. We conclude that Salmonella virulence factors and antibiotic treatment promote pathogen expansion through the same mechanism: depletion of butyrate-producing Clostridia to elevate epithelial oxygenation, allowing aerobic Salmonella growth. äDepletion of butyrate-producing Clostridia from the gut microbiota dri(epmc).pdf DeepDyve Pubget Overpricing