Chronic inflammation in the etiology of disease across the life span

• Type of Material: Article
• Authors: David Furman, Stanford University; Judith Campisi, Buck Institute for Research on Aging; Eric Verdin, Buck Institute for Research on Aging; Pedro Carrera-Bastos, Lund University; Sasha Targ, Iuve Inc; Claudio Franceschi, Lobachevsky University; Luigi Ferrucci, National Institute on Aging; Derek W. Gilroy, University College London; Alessio Fasano, Harvard University; Gary Miller, Emory University; Andrew Miller, Emory University; Alberto Mantovani, Humanitas Clinical and Research Center, Rozzano; Cornelia M. Weyand, Stanford University; Nir Barzilai, Albert Einstein College of Medicine; Jorg J. Goronzy, Stanford University; Thomas A. Rando, Stanford University; Rita B. Effros, University of California Los Angeles; Alejandro Lucia, European University of Madrid; Nicole Kleinstreuer, National Institute of Environmental Health Sciences; George M. Slavich, University of California Los Angeles
• Language: English
• Date: 2019-12-01
• Publisher: Nature
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © Springer Nature America, Inc. 2019.
• Final Published Version (URL): http://dx.doi.org/10.1038/s41591-019-0675-0
• Title of Journal or Parent Work: Nature Medicine
• Volume: 25
• Issue: 12
• Start Page: 1822
• End Page: 1832
• Grant/Funding Information: National Institute on Aging, Glenn and SENS Foundations, and the Buck Institute for Research on Aging to J.C.; the Ministry of Education and Science of the Russian Federation Agreement (074-02-2018-330) and Horizon 2020 Framework Programme (634821, PROPAG-AGING) and JPco-fuND (ADAGE) to C.F.; Society in Science-Branco Weiss Fellowship, NARSAD Young Investigator Grant 23958 from the Brain & Behavior Research Foundation and NIH grant (K08 MH103443) to G.M.S.; Intramural Research Program of the National Institute of Aging, NIH to L.F.; the MRC (UK) and Wellcome Trust to D.W.G.; NIH grant (R01 DK104344) to A.F.; the European Research Commission (PHII-669415), Associazione Italiana Ricerca sul Cancro (Projects IG 19014, 5×1000 9962 and 21147), Fondazione Cariplo, and Italian Ministry of Health to A.M.; This work was made possible by support from the National Institutes of Health (NIH) and the Buck Institute for Research on Aging to D.F.; NIH grant (P01 AG036695) to T.A.R.; the National Institute on Aging and UCLA AIDS Institute to R.B.E.; the Spanish Ministry of Economy and Competitiveness and Fondos FEDER (PI15/00558 and PI18/00139) to A.L.
• Keywords: Supplementation; Cell Biology; Cellular senescence; Science & Technology; Health consequences; Life Sciences & Biomedicine; Coronary heart disease; Diabetes mellitus; Adipose tissue; Biochemistry & Molecular Biology; Research & Experimental Medicine; Secretory phenotype; Immune system; C-reactive protein; Medicine, Research & Experimental; Physical activity
• Research Categories: Chemistry, Biochemistry; Health Sciences, Immunology; Biology, Cell; Biology, Molecular

Abstract

Although intermittent increases in inflammation are critical for survival during physical injury and infection, recent research has revealed that certain social, environmental and lifestyle factors can promote systemic chronic inflammation (SCI) that can, in turn, lead to several diseases that collectively represent the leading causes of disability and mortality worldwide, such as cardiovascular disease, cancer, diabetes mellitus, chronic kidney disease, non-alcoholic fatty liver disease and autoimmune and neurodegenerative disorders. In the present Perspective we describe the multi-level mechanisms underlying SCI and several risk factors that promote this health-damaging phenotype, including infections, physical inactivity, poor diet, environmental and industrial toxicants and psychological stress. Furthermore, we suggest potential strategies for advancing the early diagnosis, prevention and treatment of SCI.