期刊
CELL HOST & MICROBE
卷 21, 期 4, 页码 455-+出版社
CELL PRESS
DOI: 10.1016/j.chom.2017.03.002
关键词
-
资金
- Ontario Graduate Scholarship
- Canadian Thoracic Society
- Canadian Institutes of Health Research (CIHR)
- Early Researcher Award from the Ontario Ministry of Research and Innovation
- CIHR [FRN 123404, 224026, MOP 142773]
- McMaster Immunology Research Centre (MIRC)
- M.G. DeGroote Institute for Infectious Disease Research (IIDR)
- Medical Research Council [G1002046] Funding Source: researchfish
- MRC [G1002046] Funding Source: UKRI
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 germfree 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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据