Journal
JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES
Volume 71, Issue 9, Pages 1131-1140Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/gerona/glv151
Keywords
Adipokines; Aging; Cytokines; Infrapatellar fat pad; Osteoarthritis
Categories
Funding
- National Center for Research Resources [RR018758]
- National Institute of General Medical Sciences [GM103441]
- National Institute of Arthritis and Musculoskeletal and Skin Diseases [AR066828]
- National Institute on Aging of the National Institutes of Health [OAIC P30 AG028716]
- Arthritis Foundation
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The infrapatellar fat pad (IFP) secretes inflammatory mediators in osteoarthritic knees, but the effect of aging on IFP inflammation is unknown. We tested the hypothesis that aging increases basal and interleukin-1 beta (IL-1 beta)-stimulated IFP inflammation in 10-, 20-, and 30-month-old male F344BN F1-hybrid rats. IFPs were cultured ex vivo for 24 hours and treated +/- 1ng/mL IL-1 beta to simulate injury-induced inflammation. IFP inflammation was evaluated by measuring secreted cytokine concentrations and by quantitative expression of immunoregulatory and pro- and anti-adipogenic genes. With age, osteoarthritis pathology increased and IFP mass decreased. Although adipocyte size did not change with age, variation in adipocyte size was positively associated with synovial thickness independent of age whereas associations with cartilage damage were age dependent. In the absence of IL-1 beta, aging was associated with a significant increase in IFP secretion of tumor necrosis factor alpha by 67% and IL-13 by 35% and a reduction in the expression of immunoregulatory M2 macrophage genes. However, following an IL-1 beta challenge, adipogenesis markers decreased and pro- and anti-inflammatory cytokines increased independent of age. The lone exception was leptin, which decreased > 70% with age. Thus, although aging promotes osteoarthritis risk by increasing basal inflammation, our findings also revealed a potentially protective effect of aging by decreasing IL-1 beta-stimulated leptin production.
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