Age-Associated Microbial Dysbiosis Promotes Intestinal Permeability, Systemic Inflammation, and Macrophage Dysfunction
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Abstract
Levels of inflammatory mediators in circulation are known to increase with age, but the underlying cause of this age-associated inflammation is debated. We find that, when maintained under germ-free conditions, mice do not display an age-related increase in circulating pro-inflammatory cytokine levels. A higher proportion of germ-free mice live to 600 days than their conventional counterparts, and macrophages derived from aged germ-free mice maintain anti-microbial activity. Co-housing germ-free mice with old, but not young, conventionally raised mice increases pro-inflammatory cytokines in the blood. In tumor necrosis factor (TNF)-deficient mice, which are protected from age-associated inflammation, age-related microbiota changes are not observed. Furthermore, age-associated microbiota changes can be reversed by reducing TNF using anti-TNF therapy. These data suggest that aging-associated microbiota promote inflammation and that reversing these age-related microbiota changes represents a potential strategy for reducing age-associated inflammation and the accompanying morbidity.
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The record
- Venue
- Cell Host & Microbe
- Topic
- Gut microbiota and health
- Field
- Biochemistry, Genetics and Molecular Biology
- Canadian institutions
- Population Health Research InstituteMcMaster University
- Funders
- Canadian Institutes of Health ResearchMedical Research CouncilCanadian Thoracic SocietyMichael G. DeGroote Institute for Infectious Disease Research, McMaster UniversityOntario Ministry of Research, Innovation and ScienceCanada Research ChairsOntario Ministry of Research and InnovationMcMaster University
- Keywords
- InflammationDysbiosisImmunologyTumor necrosis factor alphaBiologyCytokineMacrophageSystemic inflammationGut floraProinflammatory cytokine
- Has abstract in OpenAlex
- yes