Aging impairs mitochondrial respiratory capacity in classical monocytes
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...
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Veröffentlicht in: | Experimental gerontology 2018-07, Vol.108, p.112-117 |
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creator | Pence, Brandt D. Yarbro, Johnathan R. |
description | 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.
•Mitochondrial respiration in profiled in isolated human classical monocytes•Aging impairs maximal and spare mitochondrial respiratory capacity•Aging is associated with alterations in monocyte subsets |
doi_str_mv | 10.1016/j.exger.2018.04.008 |
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•Mitochondrial respiration in profiled in isolated human classical monocytes•Aging impairs maximal and spare mitochondrial respiratory capacity•Aging is associated with alterations in monocyte subsets</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Aging - immunology</subject><subject>Aging - metabolism</subject><subject>Cell Respiration</subject><subject>Female</subject><subject>Flow Cytometry</subject><subject>Humans</subject><subject>Immunity, Innate</subject><subject>Immunometabolism</subject><subject>Inflammaging</subject><subject>Inflammation</subject><subject>Inflammation - metabolism</subject><subject>Innate immunity</subject><subject>Male</subject><subject>Metabolism</subject><subject>Middle Aged</subject><subject>Mitochondria - metabolism</subject><subject>Monocytes - immunology</subject><subject>Monocytes - metabolism</subject><subject>Phagocytosis</subject><subject>Young Adult</subject><issn>0531-5565</issn><issn>1873-6815</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kDtP5DAUhS20CIbHL1hplZIm4foZp6BAaBeQkGigthznevAoiYOdWe38ewIDlFvd5jvn6H6E_KRQUaDqclPhvzWmigHVFYgKQB-QFdU1L5Wm8gdZgeS0lFLJY3KS8wYAFOP0iByzRknZsGZFbq_XYVwXYZhsSLkYwhzdSxy7FGxfJMxTSHaOaVc4O1kX5l0RxsL1NufgFmKIY3S7GfMZOfS2z3j-eU_J85_fTzd35cPj7f3N9UPphBRz6RvLa2jrGrgQ0rfOC9WCFIqrtgOvwaJnHgVl3CvQrmm4bjky7DT1lFt-Si72vVOKr1vMsxlCdtj3dsS4zYYBkxpEU9cLyveoSzHnhN5MKQw27QwF827QbMyHQfNu0IAwi8El9etzYNsO2H1nvpQtwNUewOXNv2GJZxdwdNiFhG42XQz_HXgDUd2Dxg</recordid><startdate>20180715</startdate><enddate>20180715</enddate><creator>Pence, Brandt D.</creator><creator>Yarbro, Johnathan R.</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20180715</creationdate><title>Aging impairs mitochondrial respiratory capacity in classical monocytes</title><author>Pence, Brandt D. ; Yarbro, Johnathan R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c454t-f9a370b7703445fbcf46b054636bd0f80aef2fe4123f608c9938b3e2ed81f13a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Aging - immunology</topic><topic>Aging - metabolism</topic><topic>Cell Respiration</topic><topic>Female</topic><topic>Flow Cytometry</topic><topic>Humans</topic><topic>Immunity, Innate</topic><topic>Immunometabolism</topic><topic>Inflammaging</topic><topic>Inflammation</topic><topic>Inflammation - metabolism</topic><topic>Innate immunity</topic><topic>Male</topic><topic>Metabolism</topic><topic>Middle Aged</topic><topic>Mitochondria - metabolism</topic><topic>Monocytes - immunology</topic><topic>Monocytes - metabolism</topic><topic>Phagocytosis</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pence, Brandt D.</creatorcontrib><creatorcontrib>Yarbro, Johnathan R.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Experimental gerontology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pence, Brandt D.</au><au>Yarbro, Johnathan R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Aging impairs mitochondrial respiratory capacity in classical monocytes</atitle><jtitle>Experimental gerontology</jtitle><addtitle>Exp Gerontol</addtitle><date>2018-07-15</date><risdate>2018</risdate><volume>108</volume><spage>112</spage><epage>117</epage><pages>112-117</pages><issn>0531-5565</issn><eissn>1873-6815</eissn><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.
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subjects | Adolescent Adult Aged Aged, 80 and over Aging - immunology Aging - metabolism Cell Respiration Female Flow Cytometry Humans Immunity, Innate Immunometabolism Inflammaging Inflammation Inflammation - metabolism Innate immunity Male Metabolism Middle Aged Mitochondria - metabolism Monocytes - immunology Monocytes - metabolism Phagocytosis Young Adult |
title | Aging impairs mitochondrial respiratory capacity in classical monocytes |
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