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Exp Gerontol. 2018 Jul 15;108:112-117. doi: 10.1016/j.exger.2018.04.008. Epub 2018 Apr 13.

Aging impairs mitochondrial respiratory capacity in classical monocytes.

Author information

1
School of Health Studies, University of Memphis, Memphis, TN, United States; Center for Nutraceutical and Dietary Supplement Research, University of Memphis, Memphis, TN, United States. Electronic address: bdpence@memphis.edu.
2
School of Health Studies, University of Memphis, Memphis, TN, United States.

Abstract

Aging is a critical healthcare concern, with age-related inflammation disposing individuals to a variety of diseases. Monocytes are affected by the aging process, with increased inflammation and impaired cellular functions such as phagocytosis. Mechanisms by which aging alters monocyte function are unknown, but recent research suggests that the balance of metabolic processes determine immune cell phenotype and function. Given the known association between aging and mitochondrial dysfunction in other tissues, we hypothesized that aging would impair mitochondrial function in monocytes. To test this, we isolated classical monocytes from young and older adults and tested mitochondrial function by a Seahorse assay. Aging reduced mitochondrial respiratory capacity and spare capacity in monocytes. Mitochondrial dysfunction is a potential mechanism by which aging alters monocyte phenotype and may impair inflammatory functions, especially in low-glucose environments where oxidative metabolism is necessary to meet energy demands.

KEYWORDS:

Immunometabolism; Inflammaging; Inflammation; Innate immunity; Metabolism

PMID:
29655929
DOI:
10.1016/j.exger.2018.04.008
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