Lipid-associated macrophages are more abundant in subcutaneous than visceral adipose tissue in patients with obesity.

肥胖患者的皮下脂肪组织中脂质相关巨噬细胞比内脏脂肪组织中脂质相关巨噬细胞更丰富

阅读:14
作者:Reyes-Farias Marjorie, Fernández-García Pablo, Corrales Patricia, González Lorena, Navarro-Sanagustín David, Soria-Gondek Andrea, Pellitero Silvia, Tarascó Jordi, Moreno Pau, Balibrea José M, Gatell Laia, Sumoy Lauro, Galán María, Martínez Ester, Villarroya Francesc, Cereijo Rubén, Herrero Laura, Sánchez-Infantes David
OBJECTIVE: Because white adipose tissue is infiltrated by several immune cells and their signature in individuals with obesity has not been fully characterized, we wanted to study the most abundant population, which is macrophages, a subtype of myeloid cell. METHODS: To address this objective, we performed transcriptomic analysis of subcutaneous adipose tissue (SAT)- and visceral adipose tissue (VAT)-infiltrated CD11b(+) myeloid cells from individuals with severe obesity. RESULTS: Our results showed that gene expression in human white adipose tissue-infiltrated CD11b(+) myeloid cells was depot-dependent. The expression of lipid-associated macrophage biomarkers was higher in SAT- than VAT-infiltrated CD11b(+) cells (TREM2, CD9, GPNMB, CD68). In contrast, VAT-infiltrated CD11b(+) cells overexpressed genes associated with a perivascular M2-like adipose tissue macrophage signature (LYVE1, TIMD4, MRC1). In addition, no classical gene expression polarization (M1 and M2) was shown when VAT and SAT CD11b(+) cells were compared. Finally, high levels of CD248, a sensor of lipids associated with insulin resistance, were found to be overexpressed in SAT- compared with VAT-infiltrated CD11b(+) myeloid cells. CONCLUSIONS: This study characterizes for the first time the macrophage biomarker signature in human VAT- and SAT-infiltrated CD11b(+) myeloid cells from individuals with severe obesity. Further studies are required to elucidate their potential role and specific function in the immunometabolism of individuals with obesity.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。