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Nat Med. 2019 Dec;25(12):1822-1832. doi: 10.1038/s41591-019-0675-0. Epub 2019 Dec 5.

Chronic inflammation in the etiology of disease across the life span.

Author information

1
Buck Institute for Research on Aging, Novato, CA, USA. furmand@stanford.edu.
2
Stanford 1000 Immunomes Project, Institute for Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, CA, USA. furmand@stanford.edu.
3
Institute for Research in Translational Medicine, Universidad Austral, CONICET, Pilar, Buenos Aires, Argentina. furmand@stanford.edu.
4
Iuve Inc., San Mateo, CA, USA. furmand@stanford.edu.
5
Buck Institute for Research on Aging, Novato, CA, USA.
6
Lawrence Berkeley National Laboratory, Berkeley, CA, USA.
7
Center for Primary Health Care Research, Lund University/Region Skåne, Skåne University Hospital, Malmö, Sweden.
8
Iuve Inc., San Mateo, CA, USA.
9
Medical Scientist Training Program, University of California, San Francisco, San Francisco, CA, USA.
10
IRCCS Institute of Neurological Sciences of Bologna, Bologna, Italy.
11
Department of Applied Mathematics and Laboratory of Systems Biology of Aging, Lobachevsky University, Nizhny Novgorod, Russia.
12
Translational Gerontology Branch, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
13
Centre for Clinical Pharmacology and Therapeutics, Division of Medicine, University College London, London, UK.
14
MassGeneral Hospital for Children, Harvard Medical School, Boston, MA, USA.
15
Department of Environmental Health Sciences, School of Public Health, Columbia University Medical Center, New York, NY, USA.
16
Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA, USA.
17
Humanitas Clinical and Research Center, Rozzano, Milan, Italy.
18
Department of Biomedical Sciences, Humanitas University, Pieve Emanuele, Milan, Italy.
19
William Harvey Research Institute, Barts and the London School of Medicine, Queen Mary University, London, UK.
20
Division of Immunology and Rheumatology, Department of Medicine, Stanford University, Stanford, CA, USA.
21
Departments of Medicine and Genetics, Albert Einstein College of Medicine, New York, NY, USA.
22
Paul F. Glenn Center for the Biology of Aging, Stanford University School of Medicine, Stanford, CA, USA.
23
Center for Tissue Regeneration, Repair and Restoration, Veterans Affairs Palo Alto Health Care System, Palo Alto, CA, USA.
24
Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
25
Department of Pathology, University of California, Los Angeles, Los Angeles, CA, USA.
26
Faculty of Sport Sciences, Universidad Europea de Madrid, Madrid, Spain.
27
Research Institute of the Hospital 12 de Octubre (i+12), Madrid, Spain.
28
Biostatistics and Computational Biology Branch, Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, NC, USA.
29
NTP Interagency Center for the Evaluation of Alternative Toxicological Methods, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, NC, USA.
30
Cousins Center for Psychoneuroimmunology and Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, Los Angeles, CA, USA.

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.

PMID:
31806905
DOI:
10.1038/s41591-019-0675-0

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