title: Interferon tau alleviates obesity-induced adipose tissue inflammation and insulin resistance by regulating macrophage polarization.
abstract: Chronic adipose tissue inflammation is a hallmark of obesity-induced insulin resistance and anti-inflammatory agents can benefit patients with obesity-associated syndromes. Currently available type I interferons for therapeutic immunomodulation are accompanied by high cytotoxicity and therefore in this study we have examined anti-inflammatory effects of interferon tau (IFNT), a member of the type I interferon family with low cellular toxicity even at high doses. Using a diet-induced obesity mouse model, we observed enhanced insulin sensitivity in obese mice administered IFNT compared to control mice, which was accompanied by a significant decrease in secretion of proinflammatory cytokines and elevated anti-inflammatory macrophages (M2) in adipose tissue. Further investigations revealed that IFNT is a potent regulator of macrophage activation that favors anti-inflammatory responses as evidenced by activation of associated surface antigens, production of anti-inflammatory cytokines, and activation of selective cell signaling pathways. Thus, our study demonstrates, for the first time, that IFNT can significantly mitigate obesity-associated systemic insulin resistance and tissue inflammation by controlling macrophage polarization, and thus IFNT can be a novel bio-therapeutic agent for treating obesity-associated syndromes and type 2 diabetes.
authors.affiliation: Department of Animal Science, Texas A&M University, College Station, Texas, United States of America.
authors.forename: Wei
authors.initials: W
authors.lastname: Ying
authors.affiliation: Department of Veterinary Physiology and Pharmacology, College of Veterinary Medicine & Biomedical Sciences, Texas A&M University, College Station, Texas, United States of America.
authors.forename: Srikanth
authors.initials: S
authors.lastname: Kanameni
authors.affiliation: Department of Veterinary Physiology and Pharmacology, College of Veterinary Medicine & Biomedical Sciences, Texas A&M University, College Station, Texas, United States of America.
authors.forename: Cheng-An
authors.initials: CA
authors.lastname: Chang
authors.affiliation: Department of Veterinary Physiology and Pharmacology, College of Veterinary Medicine & Biomedical Sciences, Texas A&M University, College Station, Texas, United States of America.
authors.forename: Vijayalekshmi
authors.initials: V
authors.lastname: Nair
authors.affiliation: Department of Veterinary Physiology and Pharmacology, College of Veterinary Medicine & Biomedical Sciences, Texas A&M University, College Station, Texas, United States of America.
authors.forename: Stephen
authors.initials: S
authors.lastname: Safe
authors.affiliation: Department of Animal Science, Texas A&M University, College Station, Texas, United States of America.
authors.forename: Fuller W
authors.initials: FW
authors.lastname: Bazer
authors.affiliation: Department of Veterinary Physiology and Pharmacology, College of Veterinary Medicine & Biomedical Sciences, Texas A&M University, College Station, Texas, United States of America.
authors.forename: Beiyan
authors.initials: B
authors.lastname: Zhou
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects* / Q000276:immunology*; D000818:Animals; D059305:Diet, High-Fat / Q000009:adverse effects; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D007333:Insulin Resistance / Q000276:immunology*; D007370:Interferon Type I / Q000494:pharmacology*; D008262:Macrophage Activation / Q000187:drug effects; D008264:Macrophages / Q000166:cytology* / Q000187:drug effects* / Q000276:immunology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000276:immunology* / Q000473:pathology; D011257:Pregnancy Proteins / Q000494:pharmacology*
chemical_list: D007370:Interferon Type I; D011257:Pregnancy Proteins; C020947:interferon tau