title: Gut microbiota from metabolic disease-resistant, macrophage-specific RIP140 knockdown mice improves metabolic phenotype and gastrointestinal integrity.
abstract: While fecal microbiota transplantation (FMT) presents an attractive therapeutic strategy, it remains unclear how to choose the microbiota repertoire that most effectively transfers benefit to recipients. We identified a beneficial taxonomic repertoire in a transgenic mouse model (RIP140mϕKD) which resists the development of high fat diet (HFD)-induced metabolic diseases due to enhanced anti-inflammation engineered by lowering receptor interacting protein (RIP140) expression in macrophage. We confirmed using FMT from HFD-fed RIP140mϕKD to wild type (WT) mice that recipient mice acquired the microbiota repertoire of donor mice. Importantly, FMT from RIP140mϕKD to WT not only effectively transferred the beneficial taxonomic repertoire to WT recipients, but also enabled recipient animals acquiring the anti-inflammatory status of RIP140mϕKD donor animals and avoid HFD-induced insulin resistance, which is associated with significantly improved intestinal integrity. We conclude that FMT can transfer not only microbiota but also the donors' intestinal innate immune status and improved intestinal integrity.
authors.affiliation: Department of Pharmacology, University of Minnesota Medical School, Minneapolis, MN 55455, USA.
authors.forename: Yi-Wei
authors.initials: YW
authors.lastname: Lin
authors.affiliation: Department of Computer Science and Engineering, University of Minnesota, Minneapolis, Minnesota 55455, USA.|Université de Nantes, EA 3826 Thérapeutiques cliniques et expérimentales des infections. Faculté de médecine, 1 Rue G Veil, 44000 Nantes, France.
authors.forename: Emmanuel
authors.initials: E
authors.lastname: Montassier
authors.affiliation: Department of Computer Science and Engineering, University of Minnesota, Minneapolis, Minnesota 55455, USA.|Biotechnology Institute, University of Minnesota, Saint Paul, Minnesota, 55108, USA.
authors.forename: Dan
authors.initials: D
authors.lastname: Knights
authors.affiliation: Department of Pharmacology, University of Minnesota Medical School, Minneapolis, MN 55455, USA.
authors.forename: Li-Na
authors.initials: LN
authors.lastname: Wei
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000235:genetics*; D000818:Animals; D004032:Diet / Q000009:adverse effects; D060467:Disease Resistance; D004734:Energy Metabolism; D000069467:Fecal Microbiota Transplantation; D000069196:Gastrointestinal Microbiome; D056726:Genetic Association Studies; D005838:Genotype; D008264:Macrophages / Q000378:metabolism*; D008297:Male; D008659:Metabolic Diseases / Q000175:diagnosis / Q000209:etiology* / Q000378:metabolism* / Q000628:therapy; D051379:Mice; D018345:Mice, Knockout; D009687:Nuclear Proteins / Q000235:genetics*; D000078723:Nuclear Receptor Interacting Protein 1; D010641:Phenotype
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D009687:Nuclear Proteins; D000078723:Nuclear Receptor Interacting Protein 1