Not all macrophages are harmful in obesity
InFLAMES Flagship researchers at University of Turku report dynamic responses of multiple different macrophage types in white adipose tissue during the development and treatment of obesity.
Over 20 % of European adults are obese, and obesity is a major risk factor for several chronic diseases, including diabetes, cardiovascular diseases, and cancer. Macrophages, a type of immune cell, are known to have a central contribution to obesity-associated chronic inflammation in adipose tissue, but the roles of the different macrophage types have remained elusive. The new study, led by Academy Research Fellow Pia Rantakari and Professor Marko Salmi, dissected the heterogeneity and functions of tissue-resident macrophages in normal and obese white adipose tissue by using advanced single-cell proteomics technologies.
–We found that during the development of obesity as well as during dietary and pharmacological anti-obesity treatments, the embryonic-derived macrophage populations remained quite stable. In contrast, adult bone marrow-derived macrophage types showed strong dynamic responses according to metabolic challenges, says Doctoral Candidate Inês Félix.
–Our findings have vital implications for the rational design of macrophage-targeting immunotherapies. Currently, the focus is on the broad-scale inhibition of macrophages in adipose tissue of obese individuals. Based on our results, new strategies selectively targeting only the harmful macrophage subpopulations are needed to successfully combat obesity-associated inflammation, concludes Senior Researcher Heli Jokela.
Rantakari’s and Salmi´s research groups are part of the Academy of Finland –funded InFLAMES Flagship, a joint initiative of University of Turku and Åbo Akademi University. The goal of the Flagship is to integrate immunological and immunology-related research activities to develop and exploit new diagnostic and therapeutic tools.
The research article has been published in the Frontiers in Immunology publication series.