Lipocalin-2 resistance confers an advantage to Salmonella enterica serotype Typhimurium for growth and survival in the inflamed intestine. Molecular and phenotypic analysis of the CS54 island of Salmonella enterica serotype Typhimurium: identification of intestinal colonization and persistence determinants. Salmonella uses energy taxis to benefit from intestinal inflammation. A two-component regulatory system ( phoP phoQ) controls Salmonella typhimurium virulence. Ethanolamine utilization in Salmonella typhimurium: nucleotide sequence, protein expression, and mutational analysis of the cchA cchB eutE eutJ eutG eutH gene cluster. Analysis of the genome structure of the nonpathogenic probiotic Escherichia coli strain Nissle 1917. Quality control for plant metabolomics: reporting MSI-compliant studies. Contribution of flagellin pattern recognition to intestinal inflammation during Salmonella enterica serotype Typhimurium infection. MudSacI, a transposon with strong selectable and counterselectable markers: use for rapid mapping of chromosomal mutations in Salmonella typhimurium. Global dissemination of extensively drug-resistant carbapenemase-producing Enterobacteriaceae: clinical perspectives on detection, treatment and infection control. Alteration of gut microbiota by vancomycin and bacitracin improves insulin resistance via glucagon-like peptide 1 in diet-induced obesity. Antibiotic-induced shifts in the mouse gut microbiome and metabolome increase susceptibility to Clostridium difficile infection. Ecological mechanism controlling growth of Escherichia coli in continuous flow cultures and in the mouse intestine. Organocatalytic oxidations mediated by nitroxyl radicals. The use of TEMPO (2,2,6,6-tetramethylpiperidine- N-oxyl) for the oxidation of primary and secondary alcohols. Vascular endothelial cells synthesize nitric oxide from l-arginine. Comparison of the nitric oxide synthase inhibitors methylarginine and aminoguanidine as prophylactic and therapeutic agents in rat adjuvant arthritis. Streptomycin-induced inflammation enhances Escherichia coli gut colonization through nitrate respiration. Microbiota-liberated host sugars facilitate post-antibiotic expansion of enteric pathogens. Contribution of Salmonella typhimurium virulence factors to diarrheal disease in calves. Pretreatment of mice with streptomycin provides a Salmonella enterica serovar Typhimurium colitis model that allows analysis of both pathogen and host. A link between gut community metabolism and pathogenesis: molecular hydrogen-stimulated glucarate catabolism aids Salmonella virulence. Hydrogen-stimulated carbon acquisition and conservation in Salmonella enterica serovar Typhimurium. Kauffmann–White–Schema (1989) 1–171 (Bundesgesundheitsamt, 1992) Comparative analysis of Salmonella genomes identifies a metabolic network for escalating growth in the inflamed gut. Effect of streptomycin on susceptibility of intestinal tract to experimental Salmonella infection. Effect of antibiotic therapy in acute salmonellosis on the fecal excretion of salmonellae. Treatment of Salmonella gastroenteritis with ampicillin, amoxicillin, or placebo. Epidemiologic evidence that prior antimicrobial exposure decreases resistance to infection by antimicrobial-sensitive Salmonella. Our results identify host-mediated oxidation of carbohydrates in the gut as a mechanism for post-antibiotic pathogen expansion. Typhimurium used galactarate and glucarate within the gut lumen of streptomycin pre-treated mice, and genetic ablation of the respective catabolic pathways reduced S. By elevating expression of the gene encoding inducible nitric oxide synthase (iNOS) in the caecal mucosa, streptomycin treatment increased post-antibiotic availability of the oxidation products galactarate and glucarate in the murine caecum. Here we show that host-mediated oxidation of galactose and glucose promotes post-antibiotic expansion of S. enterica serovars are not fully resolved. However, the mechanisms by which streptomycin treatment drives an expansion of S. These antibiotic-induced changes in the gut microbiota can be studied in mice, in which the disruption of a balanced microbial community by treatment with the antibiotic streptomycin leads to an expansion of S.
Antibiotic usage elevates the risk of contracting gastroenteritis caused by Salmonella enterica serovars 1, increases the duration for which patients shed the pathogen in their faeces, and may on occasion produce a bacteriologic and symptomatic relapse 2, 3. Changes in the gut microbiota may underpin many human diseases, but the mechanisms that are responsible for altering microbial communities remain poorly understood.
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