The Immunological Response to Chronic Stress in Obese Mice

Abstract

Chronic stress is a major risk factor for cardiovascular disease. We have shown that chronic stress, which acts as a trigger for anxiety and depression, significantly reduces vascular function in obese rats and mice. Such vascular dysfunction is linked to an increase in systemic inflammation. The spleen and adipose tissue are major sources of these peripheral immune cells. We sought to identify the immunological changes in the spleen after chronic unpredictable stress (UCMS).Spleen and gonadal adipose tissue immune cells from male obese mice who underwent either 8 weeks of non‐UCMS (controls, n=6) or UCMS (n=6) for 5 days/week/7Hrs/day to elicit a depressive phenotype were analyzed by flow cytometry.Spleen size was 23% lower (p=0.08) in the UCMS group vs. controls, yet the body weight for the UCMS mice was reduced compared to obese controls (48±0.7 vs. 42±0.8, p<0.01), resulting in no differences in the ratio of spleen/body weight. To evaluate and quantify changes in the cellular immune composition of the spleen with UCMS, we harvested spleens from control and UCMS obese mice. UCMS mice tended to have lower numbers of CD45 compared to controls. Although no differences in CD8, CD4 or the CD4/CD8 ratio, or B‐cells were noted, the number of M2 macrophages were generally lower in the UCMS vs. control group, with no differences in M1 macrophages. In the visceral adipose tissue, CD45+ cells were lower in the UCMS group, which was accompanied by a lower number of CD8+ and CD4+ cells in the UCMS groups.Our data suggests that chronic stress in obese mice alters the immune cell populations in the spleen and visceral fat of obese mice. Given that these tissues play an important role in the release of immune cells into the systemic circulation, the immune changes could play an important role on the vascular dysfunction noted in our mice with exposure to chronic stress.Support or Funding InformationOD016165 (KB)This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.