title: Respiration of Microbiota-Derived 1,2-propanediol Drives Salmonella Expansion during Colitis.
abstract: Intestinal inflammation caused by Salmonella enterica serovar Typhimurium increases the availability of electron acceptors that fuel a respiratory growth of the pathogen in the intestinal lumen. Here we show that one of the carbon sources driving this respiratory expansion in the mouse model is 1,2-propanediol, a microbial fermentation product. 1,2-propanediol utilization required intestinal inflammation induced by virulence factors of the pathogen. S. Typhimurium used both aerobic and anaerobic respiration to consume 1,2-propanediol and expand in the murine large intestine. 1,2-propanediol-utilization did not confer a benefit in germ-free mice, but the pdu genes conferred a fitness advantage upon S. Typhimurium in mice mono-associated with Bacteroides fragilis or Bacteroides thetaiotaomicron. Collectively, our data suggest that intestinal inflammation enables S. Typhimurium to sidestep nutritional competition by respiring a microbiota-derived fermentation product.
authors.affiliation: Department of Medial Microbiology and Immunology, School of Medicine, University of California Davis, Davis, CA, United States of America.
authors.forename: Franziska
authors.initials: F
authors.lastname: Faber
authors.affiliation: Department of Microbiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
authors.forename: Parameth
authors.identifier: 0000-0002-6339-8744
authors.initials: P
authors.lastname: Thiennimitr
authors.affiliation: Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.
authors.forename: Luisella
authors.initials: L
authors.lastname: Spiga
authors.affiliation: Department of Medial Microbiology and Immunology, School of Medicine, University of California Davis, Davis, CA, United States of America.
authors.forename: Mariana X
authors.initials: MX
authors.lastname: Byndloss
authors.affiliation: Department of Medial Microbiology and Immunology, School of Medicine, University of California Davis, Davis, CA, United States of America.
authors.forename: Yael
authors.identifier: 0000-0002-0183-2816
authors.initials: Y
authors.lastname: Litvak
authors.affiliation: Department of Veterinary Pathobiology, College of Veterinary Medicine, Texas A&M University, College Station, TX, United States of America.
authors.forename: Sara
authors.identifier: 0000-0001-9154-8909
authors.initials: S
authors.lastname: Lawhon
authors.affiliation: Department of Microbial Pathogenesis and Immunology, College of Medicine, Texas A&M University Health Science Center, Bryan, TX, United States of America.
authors.forename: Helene L
authors.initials: HL
authors.lastname: Andrews-Polymenis
authors.affiliation: Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.
authors.forename: Sebastian E
authors.initials: SE
authors.lastname: Winter
authors.affiliation: Department of Medial Microbiology and Immunology, School of Medicine, University of California Davis, Davis, CA, United States of America.
authors.forename: Andreas J
authors.initials: AJ
authors.lastname: Bäumler
mesh_terms: D000818:Animals; D019069:Cell Respiration / Q000502:physiology; D003092:Colitis / Q000382:microbiology*; D004195:Disease Models, Animal; D054884:Host-Pathogen Interactions / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D016133:Polymerase Chain Reaction; D019946:Propylene Glycol / Q000378:metabolism*; D012481:Salmonella Infections, Animal / Q000378:metabolism*; D012486:Salmonella typhimurium / Q000254:growth & development / Q000472:pathogenicity*; D037521:Virulence Factors / Q000378:metabolism
chemical_list: D037521:Virulence Factors; D019946:Propylene Glycol