title: Deletion of the Toll-Like Receptor 5 Gene Per Se Does Not Determine the Gut Microbiome Profile That Induces Metabolic Syndrome: Environment Trumps Genotype.
abstract: Over the past decade, emerging evidence has linked alterations in the gut microbial composition to a wide range of diseases including obesity, type 2 diabetes, and cardiovascular disease. Toll-like receptors (TLRs) are the major mediators for the interactions between gut microbiota and host innate immune system, which is involved in the localization and structuring of host gut microbiota. A previous study found that TLR5 deficient mice (TLR5KO1) had altered gut microbial composition which led to the development of metabolic syndrome including hyperlipidemia, hypertension, insulin resistance and increased adiposity. In the current study, a second TLR5-deficient mouse model was studied (TLR5KO2). TLR5 deficient mice did not manifest metabolic abnormalities related to the metabolic syndrome compared with littermate controls maintained on normal chow or after feeding a high fat diet. Analysis of the gut microbial composition of littermate TLR5KO2 and wild type mice revealed no significant difference in the overall microbiota structure between genotypes. However, the TLR5KO2 microbiota was distinctly different from that previously reported for TLR5KO1 mice with metabolic syndrome. We conclude that an altered composition of the microbiota in a given environment can result in metabolic syndrome, but it is not a consequence of TLR5 deficiency per se.
authors.affiliation: Department of Nutrition Sciences, School of Health Professions, the University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
authors.forename: Wei
authors.initials: W
authors.lastname: Zhang
authors.affiliation: Department of Medical Microbiology and Infectious Diseases, University of Manitoba, Winnipeg, Canada.
authors.forename: Riley
authors.initials: R
authors.lastname: Hartmann
authors.affiliation: Department of Animal Science, University of Manitoba, Winnipeg, Canada.
authors.forename: Hein Min
authors.initials: HM
authors.lastname: Tun
authors.affiliation: Division of Gastroenterology and Hepatology, School of Medicine, the University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
authors.forename: Charles O
authors.initials: CO
authors.lastname: Elson
authors.affiliation: Department of Medical Microbiology and Infectious Diseases, University of Manitoba, Winnipeg, Canada.|Department of Animal Science, University of Manitoba, Winnipeg, Canada.
authors.forename: Ehsan
authors.initials: E
authors.lastname: Khafipour
authors.affiliation: Department of Nutrition Sciences, School of Health Professions, the University of Alabama at Birmingham, Birmingham, Alabama, United States of America.|Birmingham VA Medical Center, Birmingham, Alabama, United States of America.
authors.forename: W Timothy
authors.initials: WT
authors.lastname: Garvey
mesh_terms: D000818:Animals; D001419:Bacteria / Q000145:classification / Q000235:genetics; D001786:Blood Glucose / Q000378:metabolism; D001823:Body Composition / Q000235:genetics; D001835:Body Weight / Q000235:genetics; D004435:Eating / Q000235:genetics; D004777:Environment; D000069196:Gastrointestinal Microbiome / Q000235:genetics*; D017353:Gene Deletion; D055786:Gene Knockout Techniques; D059647:Gene-Environment Interaction; D005838:Genotype; D005951:Glucose Tolerance Test; D007113:Immunity, Innate / Q000235:genetics; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000235:genetics; D008055:Lipids / Q000097:blood; D024821:Metabolic Syndrome / Q000235:genetics* / Q000276:immunology / Q000382:microbiology*; D051379:Mice; D051198:Toll-Like Receptor 5 / Q000172:deficiency / Q000235:genetics*
chemical_list: D001786:Blood Glucose; D007328:Insulin; D008055:Lipids; D051198:Toll-Like Receptor 5