Presenting Author: Ahmed Rakib
, Graduate Research Assistant at Univ. of Tennessee Hlth. Sci.Ctr.
Abstract:
Obesity is associated with chronic low-grade adipose tissue (AT) inflammation and contributes to metabolic disorders. AT macrophages are a major source of proinflammatory mediators and aggravate adipocyte dysfunction during obesity. The sialic acid-binding Ig-like lectin E (Siglec-E) is expressed in macrophages and regulates immune function, yet the role of Siglec-E in obesity-associated inflammation has not been reported. Thus, we investigated the role of Siglec-E in mediating AT inflammation. We fed a normal diet (ND) and high-fat diet (HFD) to wild-type (WT) and Siglec-E knockout mice (Siglec-E-/-) for 12 weeks. The HFD consumption increased the body weight of both WT and Siglec-E-/-, metabolic markers, and lipid profile as compared to ND-fed mice. Further, infiltration of CD11b+CD11c+ and CD11b+F4/80+ M1 macrophages increased in both WT and Siglec-E-/- HFD-fed mice. Correspondingly, an increase in IFN-γ, IL-6, iNOS, and TNF-α in macrophages was noticed in the HFD-fed Siglec-E-/- mice. In addition, adipogenic and inflammatory markers, including Arg1, PPARγ, UCP1, and FASN in the monocytic myeloid-derived suppressor cells are increased in HFD-fed Siglec-E-/- mice as compared to the WT mice. The expression of adaptor molecules of non-canonical NF-κB and TRAF3 signaling is increased in AT of HFD-fed Siglec-E-/- mice as compared to WT mice. This study supports the notion that modulating Siglec-E alters TRAF3 signaling to suppress AT inflammation during obesity.
Siglec-E modulates TRAF3 signaling to protect from obesity-induced adipose tissue inflammation
Category
Poster and Podium (Block Symposium)
Description
Custom CSS
double-click to edit, do not edit in source
Date: May 5 Presentation Time: 03:15 PM to 04:30 PM Room: Exhibit Hall F1