PRACA ORYGINALNA
Aktywność sekrecyjna podskórnej tkanki tłuszczowej brzusznej u mężczyzn chorych na reumatoidalne zapalenie stawów i chorobę zwyrodnieniową stawów - powiązanie z danymi klinicznymi i laboratoryjnymi.
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Data nadesłania: 15-09-2016
Data ostatniej rewizji: 17-10-2016
Data akceptacji: 17-10-2016
Data publikacji online: 28-11-2016
Data publikacji: 28-10-2016
Reumatologia 2016;54(5):227-235
SŁOWA KLUCZOWE
DZIEDZINY
STRESZCZENIE
Introduction: Adipose tissue exerts widespread effects on the metabolism and immune system, but its activity differs between the genders. In the general population low-grade adipose tissue inflammation contributes to development of diseases of affluence. Little is known about the systemic impact of peripheral fat tissue in osteoarthritis (OA) and rheumatoid arthritis (RA), characterized by chronic, low- and high-grade systemic inflammation, respectively. To clarify this we evaluated the secretory activity of subcutaneous abdominal adipose tissue (SAAT) obtained from male patients affected with RA (n = 21) and OA (n = 13), and assessed its association with body mass and composition, demographic, clinical and laboratory data.
Material and methods: Basal and interleukin (IL)-1β-triggered secretion of selected adipocytokines from SAAT explants was measured by specific enzyme-linked immunosorbent assays (ELISA). Patients’ body composition was evaluated by bioelectric impendence technique.
Results: Rheumatoid SAAT secreted more adiponectin and macrophage migration inhibitory factor (MIF) than respective osteoarthritis tissue. In both RA and OA patient groups, stimulation of SAAT explants with IL-1β(1 ng/ml/100 mg tissue) significantly up-regulated release of pro-(IL-6, IL-8, tumor necrosis factor – TNF) and anti-inflammatory (IL-10) cytokines but had no effect on the secretion of adiponectin, leptin, MIF and hepatocyte growth factor (HGF). Compared with RA, patients with OA were more obese. In RA patients SAAT-released adiponectin and TNF inversely correlated with body mass index (BMI) and visceral fat rating (FVSC). In addition, SAAT-secreted adiponectin and leptin positively correlated with DAS28 and disease duration, respectively. In the OA group tissue-released TNF positively correlated with patients’ age.
Conclusions: We conclude that in RA male patients adipocytokines originating from SAAT are of clinical importance because: (i) adiponectin and TNF may contribute to maintenance of normal body composition and mass, (ii) in addition adiponectin may play a pathogenic role. Moreover, in both RA and OA male patients secretory activity of SAAT may vary with time.
REFERENCJE (28)
1.
Kontny E. Pathogenesis of rheumatoid arthritis. Part I: Acquired immunity, genetic and environmental factors. Reumatologia 2011; 49: 47-54.
2.
Kontny E. Pathogenesis of rheumatoid arthritis. Part II: Innate immunity, new therapeutic targets. Reumatologia 2011; 49: 115-121.
3.
Kontny E. Pathogenesis of rheumatoid arthritis. Part III: Cytokines and joint destruction. Reumatologia 2011; 49: 180-186.
4.
Cutolo M, Kitas GD, van Riel PL. Burden of disease in treated rheumatoid arthritis patients: going beyond the joint. Semin Arthritis Rheum 2014; 43: 479-488.
5.
Berenbaum F. Osteoarthritis as an inflammatory disease (osteoarthritis is not osteoarthrosis). Osteoarthritis Cartilage 2013; 21: 16-21.
6.
van Dijk GM, Veenhof C, Schellevis F, et al. Comorbidity, limitations in activities and pain in patients with osteoarthritis of the hip or knee. BMC Musculoskelet Disord 2008; 9: 95.
7.
Johnson VL, Hunter DJ. The epidemiology of osteoarthritis. Best Pract Res Clin Rheumatol 2014; 28: 5-15.
8.
Masuko K. Rheumatoid cachexia revised: a metabolic co-morbidity in rheumatoid arthritis. Front Nutr 2014; 1: 20.
9.
Versini M, Jeandel PY, Rosenthal E, Shoenfeld Y. Obesity in autoimmune diseases: not a passive bystander. Autoimmun Rev 2014; 13: 981-1000.
10.
Conde J, Scotece M, López V, et al. Adipokines: novel players in rheumatic diseases. Discov Med 2013; 15: 73-83.
11.
Kontny E, Plebanczyk M, Lisowska B, et al. Comparison of rheumatoid articular adipose and synovial tissue reactivity to proinflammatory stimuli: contribution to adipocytokine network. Ann Rheum Dis 2012; 71: 262-267.
12.
Eymard F, Pigenet A, Citadelle D, et al. Induction of an inflammatory and prodegenerative phenotype in autologous fibroblast-like synoviocytes by the infrapatellar fat pad from patients with knee osteoarthritis. Arthritis Rheum 2014; 66: 2165-2174.
13.
Lee MJ, Wu Y, Fried SK. Adipose tissue heterogeneity: implication of depot differences in adipose tissue for obesity complications. Mol Aspects Med 2013; 34: 1-11.
14.
Kontny E, Zielińska A, Skalska U, et al. Distinct secretory activity and clinical impact of subcutaneous abdominal adipose tissue in women with rheumatoid arthritis and osteoarthritis. Inflammation 2016 (in press).
15.
White UA, Tchoukalova YD. Sex dimorphism and depot differences in adipose tissue function. Biochim Biophys Acta 2014; 1842: 377-392.
16.
Arnett FC, Edworthy SM, Bloch DA, et al. The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum 1988; 31: 315-324.
17.
Gustafson B. Adipose tissue, inflammation and atherosclerosis. J Atheroscler Thromb 2010; 17: 332-341.
18.
Lee BC, Lee J. Cellular and molecular players in adipose tissue inflammation in the development of obesity-induced insulin resistance. Biochim Biophys Acta 2014; 1842: 446-462.
19.
Kontny E, Prochorec-Sobieszek M. Articular adipose tissue resident macrophages in rheumatoid arthritis patients: potential contribution to local abnormalities. Rheumatology (Oxford) 2013; 52: 2158-2167.
20.
Jéquier E. Leptin signalling, adiposity, and energy balance. Ann N Y Acad Sci 2002; 967: 379-388.
21.
Dridi S, Taouis M. Adiponectin and energy homeostasis: consensus and controversy. J Nutr Biochem 2009; 20: 831-839.
22.
Morrison MC, Kleemann R. Role of macrophage migration inhibitory factor in obesity, insulin resistance, type 2 diabetes, and associated hepatic co-morbidities: a comprehensive review of human and rodent studies. Front Immunol 2015; 6: 308.
23.
Zernecke A, Bernhagen J, Weber C. Macrophage migration inhibitory factor in cardiovascular disease. Circulation 2008; 117: 1594-1602.
24.
Benigni F, Atsumi T, Calandra T, et al. The proinflammatory mediator macrophage migration inhibitory factor induces glucose catabolism in muscle. J Clin Invest 2000; 106: 1291-1300.
25.
Batista ML Jr, Neves RX, Peres SB, et al. Heterogenous time-dependent response of adipose tissue during the development of cancer cachexia. J Endocrinol 2012; 215: 363-373.
26.
Scotece M, Conde J, López V, et al. Adiponectin and leptin: new targets in inflammation. Basic Clin Pharmacol Toxicol 2014; 114: 97-102.
27.
Frommer KW, Schäffler A, Büchler C, et al. Adiponectin isoforms: a potential therapeutic target in rheumatoid arthritis? Ann Rheum Dis 2012; 71: 1724-1732.
28.
Kontny E, Janicka I, Skalska U, Maśliński W. The effect of multimeric adiponectin isoforms and leptin on the function of rheumatoid fibroblast-like synoviocytes. Scand J Rheumatol 2015; 44: 363-368.
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