Abstract
Background: Aging (middle age) is usually associated with obesity and progressive low-grade inflammation in adipose tissue. However, how immune components in adipose tissue respond to aging is still not fully uncovered. Here, we sought to examine immune cells and inflammation in adipose tissue in aging mice. Methods: Bodyweight and insulin sensitivity were measured in 12-month-old (aging) and 3-month-old (young) C57BL/6J mice on a low-fat normal diet. UCP1 expression was examined in white adipose tissue after stimulation. The immune-cell composition and phenotypes in adipose tissue were analyzed by flow cytometry. The suppressive functions of adipose tissue-resident T regulatory cells (aTregs) for conventional T cell proliferation were evaluated by CFSE-labeling proliferation assay in vitro. Results: Compared to young mice, aging mice exhibited adipose tissue expansion and insulin resistance. UCP1 was reduced in adipose tissue, indicating impaired adipose tissue browning, in aging mice compared to young mice. The frequency of resident T cells and macrophages was increased in adipose tissue of aging mice compared to those of young mice. Moreover, the Th1 subset of T cells and the M1 subset of macrophages dominated in their parent population in adipose tissue of aging mice. In contrast to diet-induced obesity that reduced aTregs, the frequency of aTregs was increased in old mice compared to young mice. However, the anti-inflammatory cytokines IL10 and inflammation-inhibitory marker CTLA4 were reduced on aTregs in aging mice than young mice. The proliferative assay showed that the suppressive capacity of Treg cell on conventional T cell proliferation was impaired in aging mice. Conclusion: Aging in mice is associated with increased aTregs, which have reduced anti-inflammatory functions and may, therefore, contribute to increased Th1 and M1 inflammation in adipose tissue, leading to metabolic disorders in aging mice. Disclosure Z. Lian: None. X. Perrard: None. C.M. Ballantyne: Consultant; Self; Abbott, Akcea Therapeutics, Amarin Corporation, Amgen, Arrowhead Pharmaceuticals, Inc., AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Corvidia, Denka-Seiken Co., Ltd., Esperion Therapeutics, Inc., Gilead Sciences, Inc., Janssen Pharmaceuticals, Inc., Matinas BioPharma, Merck & Co., Inc., Novartis Pharmaceuticals Corporation, Novo Nordisk Inc., Regeneron Pharmaceuticals, Roche Diagnostic USA, Sanofi. Research Support; Self; Abbott, Akcea Therapeutics, Amgen, Esperion Therapeutics, Inc., Novartis Pharmaceuticals Corporation, Regeneron Pharmaceuticals, Roche Diagnostic USA. H. Wu: None. Funding American Diabetes Association (1-17-IBS-082 to H.W.); National Institutes of Health (R01HL098839); American Heart Association (16GRNT30410012)
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