Work

Siglec-E modulates adipogenic and inflammatory markers to induce adipose tissue inflammation during obesity 2380

Year: 2025

Type: article

Abstract: Description Over the last five decades, the prevalence of obesity increased drastically, becoming a global epidemic. Obesity is characterized by low-grade chronic inflammation in the adipose tissue (AT). Adipocytes secrete several adipokines and chemokines, which further attract macrophages into the obese AT to induce inflammation. Reportedly, Siglec-E is expressed by macrophages and dendritic cells (DCs), orchestrates immune function. However, the role of Siglec-E in AT inflammation during obesity is not well known. To explore the role of Siglec-E in AT inflammation, we fed normal diet (ND) and high-fat diet (HFD) to wild-type (WT) and Siglec-E knockout mice (Siglec-E-/-) for 12 weeks. HFD induction increased the body weight, AT inflammation, and other metabolic markers in both WT and Siglec-E-/- mice as compared to ND. The expression of adaptor molecules of non-canonical NF-κB signaling, including TRAF3 is increased in the epididymal white AT (eWAT) and suprascapular WAT in the HFD-fed Siglec-E-/- mice as compared to WT mice. We also observed a greater increase in CD11b+CD11c+ and CD11b+F4/80+ population in BMDMs in Siglec-E-/- as compared to HFD-fed WT mice. Further, we noticed that inhibition of Siglec-E using siRNA in vitro altered the expression of adipogenic and inflammatory markers in differentiated 3T3-L1 adipocytes and RAW264.7 macrophages. Collectively, our data suggests that modulating the Siglec-E is critical for regulating AT inflammation and adipogenesis during obesity. Funding Sources This study was supported by grants from NIH (NIAID R01 AI140405) Topic Categories Cellular Adhesion, Migration, and Inflammation (CAM)

Source: The Journal of Immunology

DOI: 10.1093/jimmun/vkaf283.305