Circulation research · 2010
Interleukin-33 induces protective effects in adipose tissue inflammation during obesity in mice.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Miller Ashley M, Asquith Darren L, Hueber Axel J, Anderson Lesley A, Holmes William M, McKenzie Andrew N, Xu Damo, Sattar Naveed, McInnes Iain B, Liew Foo Y
Аннотация
RATIONALE: Chronic low-grade inflammation involving adipose tissue likely contributes to the metabolic consequences of obesity. The cytokine interleukin (IL)-33 and its receptor ST2 are expressed in adipose tissue, but their role in adipose tissue inflammation during obesity is unclear.
OBJECTIVE: To examine the functional role of IL-33 in adipose tissues and investigate the effects on adipose tissue inflammation and obesity in vivo.
METHODS AND RESULTS: We demonstrate that treatment of adipose tissue cultures in vitro with IL-33 induced production of Th2 cytokines (IL-5, IL-13, IL-10) and reduced expression of adipogenic and metabolic genes. Administration of recombinant IL-33 to genetically obese diabetic (ob/ob) mice led to reduced adiposity, reduced fasting glucose and improved glucose and insulin tolerance. IL-33 also induced accumulation of Th2 cells in adipose tissue and polarization of adipose tissue macrophages toward an M2 alternatively activated phenotype (CD206(+)), a lineage associated with protection against obesity-related metabolic events. Furthermore, mice lacking endogenous ST2 fed high-fat diet had increased body weight and fat mass and impaired insulin secretion and glucose regulation compared to WT controls fed high-fat diet.
CONCLUSIONS: In conclusion, IL-33 may play a protective role in the development of adipose tissue inflammation during obesity.
OBJECTIVE: To examine the functional role of IL-33 in adipose tissues and investigate the effects on adipose tissue inflammation and obesity in vivo.
METHODS AND RESULTS: We demonstrate that treatment of adipose tissue cultures in vitro with IL-33 induced production of Th2 cytokines (IL-5, IL-13, IL-10) and reduced expression of adipogenic and metabolic genes. Administration of recombinant IL-33 to genetically obese diabetic (ob/ob) mice led to reduced adiposity, reduced fasting glucose and improved glucose and insulin tolerance. IL-33 also induced accumulation of Th2 cells in adipose tissue and polarization of adipose tissue macrophages toward an M2 alternatively activated phenotype (CD206(+)), a lineage associated with protection against obesity-related metabolic events. Furthermore, mice lacking endogenous ST2 fed high-fat diet had increased body weight and fat mass and impaired insulin secretion and glucose regulation compared to WT controls fed high-fat diet.
CONCLUSIONS: In conclusion, IL-33 may play a protective role in the development of adipose tissue inflammation during obesity.
Предметные рубрики MeSH
AdipogenesisAdipose Tissue, WhiteAdiposityAnimalsBlood GlucoseBody WeightCells, CulturedCytokinesDisease Models, AnimalEnergy MetabolismGene Expression RegulationInflammation MediatorsInjections, IntraperitonealInsulin ResistanceInterleukin-1 Receptor-Like 1 ProteinInterleukin-33InterleukinsMacrophagesMaleMiceMice, Inbred BALB CMice, KnockoutObesityPanniculitisReceptors, InterleukinRecombinant ProteinsTh2 CellsTime Factors