IMMUNOLOGICAL PROFILE IN DIFFERENT GROUPS OF END STAGE RENAL DISEASE
DOI:
https://doi.org/10.36320/ajb/v8.i3.9297Keywords:
ESRD, IL-10, IL-17, MCP-1, TGF-β1.Abstract
Background and aim of study: End Stage Renal Disease (ESRD) is a worldwide problem in which patients are in hemo-dialysis and/or awaiting for kidney transplantation. However, the actual mechanism (s) of ESRD pathogenesis is ill-defined. The aim of this study is to investigate the role of certain immunological markers in the pathogenesis of ESRD.
Materials and methods: Sixty eight blood samples were collected from hospitalized ESRD patients with different etiology (hypertensive, diabetics, hypertensive + diabetics, and small size kidney). Twenty healthy volunteers as control group was enrolled in the study. Serum IL-10, IL-17, MCP-1 and TGF-β were estimated in all subjects.Result: A significant elevation in the serum IL-10, MCP-1 and IL-17 mean concentration in all ESRD patients groups. TGF-β mean concentration exhibited decreasing level in the hypertensive, hypertensive + diabetes and small size kidney groups and a slight elevation in the diabetes group. The IL-10: IL-17 ratio expressed elevation in all ESRD patients groups.
Conclusion: There is a progress of inflammatory reactions in all ESRD patients groups in which IL-17 and MCP-1 are playing major roles. TGF-β1 is not played its anticipated pro-fibrotic role and anti-inflammatory function in the studied group. The ratio of IL-10: IL-17 point out a slight shifting of the immunosuppressive reaction over the inflammatory reaction in all ESRD patients groups.Downloads
References
Reikes ST. Trends in end-stage renal disease. Epidemiology, morbidity and mortality. Postgrad Med., 2000; 108(1):124-126. DOI: https://doi.org/10.3810/pgm.2000.07.1152
Stenvinkel P, Ketteler M, Johnson RJ, et al. IL-10, IL-6, and TNF-α: Central factors in the altered cytokine network of uremia–the good, the bad, and the ugly. Kidney Int. 2005; 67:1216–1233. DOI: https://doi.org/10.1111/j.1523-1755.2005.00200.x
Kleinewietfeld M, Manzel A, Titze J, Kvakan H, Yosef N, Linker RA, Muller DN, Hafler DA. Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. Nature 2013, 496:518-522. DOI: https://doi.org/10.1038/nature11868
Turner JE, Paust HJ, Steinmetz OM, Panzer U. The Th17 immune response in renal inflammation. Kidney Int. 2010; 77:1070–1075. DOI: https://doi.org/10.1038/ki.2010.102
Böttinger E. TGF-B in renal injury and disease. Semin Nephrol 2007; 27: 309–320. DOI: https://doi.org/10.1016/j.semnephrol.2007.02.009
López-Hernández FJ, López-Novoa JM. Role of TGF-β in chronic kidney disease: an integration of tubular, glomerular and vascular effects. Cell Tissue Res 2012; 347:141-154. DOI: https://doi.org/10.1007/s00441-011-1275-6
Qi W, Chen X, Polhill TS, Sumual S, Twigg S, Gilbert RE, PollockCA TGF-beta1 induces IL-8 and MCP-1 through a connective tissue growth factor-independent pathway. Am J Physiol Renal Physiol., 2006; 290: F703 –F709. DOI: https://doi.org/10.1152/ajprenal.00254.2005
Segerer S, Nelson PJ & Schlöndorff D. Chemokines, chemokine receptors, and renal disease: From basic science to pathophysiologic and therapeutic studies. J Am Soc Nephrol. 2000; 11: 152−176. DOI: https://doi.org/10.1681/ASN.V111152
Said EA, Dupuy FP, Trautmann L, Zhang Y, Shi Y, et al. Programmed death-1-induced interleukin-10 production by monocytes impairs CD4+ T cell activation during HIV infection. Nature Medicine, 2010; 16 (4): 452–9. DOI: https://doi.org/10.1038/nm.2106
Tucci M, Stucci S, Strippoli S, Silvestris F. Cytokine overproduction, T-cell activation, and defective T-regulatory functions promote nephritis in systemic lupus erythematosus. J Biomed Biotechnol.2010; 2010:457146. DOI: https://doi.org/10.1155/2010/457146
Saraiva M, O'Garra A. "The regulation of IL-10 production by immune cells". Nature Reviews. Immunology, 2010; 10 (3): 170–8. DOI: https://doi.org/10.1038/nri2711
Olszyna DP, Pajkrt, D, Lauw, FN, Van Deventer, SJ. Interleukin 10 inhibits the release of CC chemokines during human endotoxemia. J Infect Dis. 2000; 181: 613–620. DOI: https://doi.org/10.1086/315275
Tomasz Porazko, Jakub Kuzniar, Mariusz Kusztal, Tomasz J. Kuzniar, Wacław Weyde, et al. IL-18 is involved in vascular injury in end-stage renal disease patients, Nephrol Dial Transplant, 2009; 24: 589–596. DOI: https://doi.org/10.1093/ndt/gfn486
El-Shafey E, El-Nagar GF, Abu Hatab H, Sabry A, and Elbaz H. Upregulation of Monocyte Chemoattractant Protein-1 (MCP-1) in Early Diabetic Nephropathy in Patients with Type-1 Diabetes Mellitus. Scholarly Research Exchange, 2015; 2008 (ID): 467264. DOI: https://doi.org/10.3814/2008/467264
van Topchii, Topchii I, Semenovykh P, Galchiskaya V, Efimova N and Scherban T, Diabetes – Clinical, Nephrology Dialysis Transplantation, 2012; 27 (2): ii167–ii177.
Ricardo SD, van GH, Eddy AA. Macrophage diversity in renal injury and repair. J Clin Invest.2008; 118: 3522–3530. DOI: https://doi.org/10.1172/JCI36150
Katz Y, Nadiv O, Beer Y. Interleukin-17 enhances tumor necrosis factor alpha-induced synthesis of interleukins 1, 6, and 8 in skin and synovial fibroblasts: a possible role as a “fine-tuning cytokine” in inflammation processes. Arthritis Rheum 2001; 44:2176-2184. DOI: https://doi.org/10.1002/1529-0131(200109)44:9<2176::AID-ART371>3.0.CO;2-4
Chun-Mei L, Rui MA, Xin-Sheng Y, Wan-Bang S, Yong L. Exploration of IL-17 amount and its correlation to CRP in the patients with MHD. Chinese Journal of Immunology, 2009-05.
Stefoni S, Cianciolo G, Donati G, Dormi A, Silvestri MG, Colì L, De Pascalis A, Iannelli S. Low TGF-beta1 serum levels are a risk factor for atherosclerosis disease in ESRD patients. Kidney Int, 2002; 61(1):324-35. DOI: https://doi.org/10.1046/j.1523-1755.2002.00119.x
Kumar A, Gupta V,Chaudhary M, Singh A, Sehajpal PK. Depleted TGF-β1 levels in End Stage Renal Disease patients from North India. Gene. 2014; 534(2):440-443 DOI: https://doi.org/10.1016/j.gene.2013.09.116
Ma L, Zhang H, Hu K, Lv G, Fu Y, Ayana D, Zhao P and Jiang Y. The imbalance between Tregs, Th17 cells and inflammatory cytokines among renal transplant recipients. BMC Immunology 2015, 16:56. DOI: https://doi.org/10.1186/s12865-015-0118-8
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