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|Title:||Lack of ST2 enhances high-fat diet-induced visceral adiposity and inflammation in BALB/c mice|
|Authors:||Pantic, Jelena |
|Journal:||Serbian Journal of Experimental and Clinical Research|
|Abstract:||Obesity and obesity-related disorders are strongly associated with a chronic low-grade infl ammation that originates from growing visceral adipose tissue during nutrient excess. Although interleukin (IL)-33 may play a protective role in obesity and atherosclerosis, the impact of the IL-33/ST2 axis on metabolic disorders needs to be further elucidated. In this study, we investigated the role of the IL-33/ST2 pathway in high-fat diet (HFD)-induced obesity using ST2- defi cient (ST2-/-) and wild type BALB/c mice. Th e deletion of ST2 enhanced systemic and visceral adipose tissue (VAT) infl ammation; ST2-/- mice that were fed a HFD for 18 weeks had experienced a signifi cantly increased weight gain and had a higher amount of total VAT. More classically activated M1 macrophages and markedly fewer alternatively activated M2 macrophages were observed in the VAT of the HFD-fed ST2-/- mice. Additionally, the VAT of the HFD-fed ST2-/- mice had an increased percentage of CD3+ T cells but fewer CD4+CD25+FoxP3+ T regulatory cells when compared to the VAT of the low-fat diet-fed controls. Th e numbers of CD3+IL-17+ and IL-5 positive VATderived mononuclear cells were signifi cantly decreased in the HFD-fed ST2-/- mice. Serum levels of the proinfl ammatory cytokines IL-1β and IFN-γ were increased in the HFDfed ST2-/- mice, while the levels of IL-6 and CRP did not diff er among the groups. Importantly, the levels of the antiinfl ammatory cytokines IL-10 and IL-13 were signifi cantly lower in the sera of the ST2-/- mice than the levelsin the sera of the wild-type controls. Our fi ndings suggest a protective role of IL33/ST2 signalling in high-fat diet-induced adipose tissue infl ammation. ST2 defi ciency related to nutrient excess is associated with the polarisation of macrophages toward the M1 phenotype and the induction of a Th 1-mediated immune response.|
|Appears in Collections:||Faculty of Medical Sciences, Kragujevac|
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