促炎细胞因子在糖尿病肾病患者中的作用
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摘要
糖尿病肾病是影响糖尿病患者生存率的重要并发症之一。其发病机制复杂,近年来通过对糖尿病肾病患者的病因的细胞和分子水平的研究发现,炎症可能是引起患者糖尿病肾病的重要病因之一。在糖尿病肾病患者的发生和发展过程中,免疫和炎症机制发挥着重要作用,炎症细胞和促炎细胞因子可以促进患者肾损伤的发展和进程,而抑制炎症反应则可以对患者的肾损伤有保护作用。本文就炎症与糖尿病肾病以及常见的促炎细胞因子与糖尿病肾病患者关系作一综述。
Diabetic nephropathy is one of the important complications to affect survival of the patients with diabetes. Its pathogenesisis is complex. In recent years,the studies on the cellular and molecular level of the cause of diabetic nephropathy found that inflammation may be one of the important factors of diabetic nephropathy. In the occurrence and development of diabetic nephropathy,immune and inflammatory mechanisms play an important role and the inflammatory cells and proinflammatory factors can promote the development of kidney damage and processes,while inhibiting the inflammatory response may have a protective effect on renal injury.In this paper,the relation of the inflammation and diabetic nephropathy,as well as the common relation of proinflammatory cytokines and diabetic nephropathy will be discussed.
Diabetic nephropathy is one of the important complications to affect survival of the patients with diabetes. Its pathogenesisis is complex. In recent years,the studies on the cellular and molecular level of the cause of diabetic nephropathy found that inflammation may be one of the important factors of diabetic nephropathy. In the occurrence and development of diabetic nephropathy,immune and inflammatory mechanisms play an important role and the inflammatory cells and proinflammatory factors can promote the development of kidney damage and processes,while inhibiting the inflammatory response may have a protective effect on renal injury.In this paper,the relation of the inflammation and diabetic nephropathy,as well as the common relation of proinflammatory cytokines and diabetic nephropathy will be discussed.
引文
[1]Atkins RC,Zimmet P.Diabetic kidney disease:act now or pay later[J].J Bras Nefrol,2010,32(1):7-10.
[2]Atkins RC.The epidemiology of chronic kidney disease[J].Kidney Int Suppl,2005,(94):S14-18.
[3]Martini S,Eichinger F,Nair V,et al.Defining human diabetic nephropathy on the molecular level:integration of transcriptomic profiles with biological knowledge[J].Rev Endocr Metab Disord,2008,9(4):267-2674.
[4]Wada J,Makino H.Inflammation and the pathogenesis of diabetic nephropathy[J].Clin Sci(Lond),2013,124(3):139-152.
[5]Lim AKH,Ma FY,Nikolic-Paterson DJ,et al.Lymphocytes promote albuminuria,but not renal dysfunction or histological damage in a mouse model of diabetic renal injury[J].Diabetologia,2010,53(8):1772-1782.
[6]Awad AS,Kinsey GR,Khutsishvili K,et al.Monocyte/macrophage chemokine receptor CCR2 mediates diabetic renal injury[J].Am J Physiol Renal Physiol,2011,301(6):F1358-1366.
[7]Navarro-Gonzalez JF,Mora-Fernandez C.The role of inflammatory cytokines in diabetic nephropathy[J].Journal of the American Society of Nephrology,2008,19(3):433-442.
[8]Mora C,Navarro JF.Inflammation and diabetic nephropathy[J].Curr Diab Rep,2006,6(6):463-468.
[9]Galkina E and Ley K.Leukocyte recruitment and vascular injury in diabetic nephropathy[J].Journal of the American Society of Nephrology,2006,17(2):368-377.
[10]Aldhahi W,Hamdy O.Adipokines,inflammation,and the endotheliumindiabetes[J].Current Diabetes Reports,2003,3(4):293-298.
[11]Pickup JC.Inflammation and activated innate immunity in the pathogenesis of type 2 diabetes[J].Diabetes Care,2004,27(3):813-823.
[12]Navarro JF,C.Mora C.Role of inflammation in diabetic complications[J].Nephrology Dialysis Transplantation,2005,20(12):2601-2604.
[13]Pickup JC,Chusney GD,Thomas SM,et al.Plasma interleukin-6,tumour necrosis factorαand blood cytokine production in type2 diabetes[J].Life Sciences,2000,67(3):291-300.
[14]Bruno G,Merletti F,Biggeri A,et al.Progression to overt nephropathy in type 2 diabetes:the casale monferrato study[J].Diabetes Care,2003,26(7):2150-2155.
[15]Spranger J,Kroke A,Mohlig M,et al.Inflammatory cytokines and the risk to develop type 2 diabetes:results of the prospective population-based European Prospective Investigation into Cancer and Nutrition(EPIC)-Potsdam Study[J].Diabetes,52(3):812-817.
[16]Hasegawa G,Nakano K,Sawada M,et al.Possible role of tumor necrosis factor and interleukin-1 in the development of diabetic nephropathy[J].Kidney International,1991,40(6):1007-1012.
[17]Navarro JF,Mora C,Macia M,et al.Inflammatory parameters are independently associated with urinary albumin in type 2 diabetes mellitus[J].The American Journal of Kidney Diseases,42(1):53-61.
[18]Dong X,Swaminathan S,Bachman LA,et al.Resident dendritic cells are the predominant TNF-secreting cell in early renal ischemiareperfusion injury[J].Kidney International,71(7):619-628.
[19]Navarro JF,Milena FJ,Mora C,et al.Renal pro-inflammatory cytokine gene expression in diabetic nephropathy:effect of angiotensin-converting enzyme inhibition and pentoxifylline administration[J].The American Journal of Nephrology,2007,26(6):562-570.
[20]Navarro JF,Mora C,Muros M,et al.Urinary tumour necrosis factor-alpha excretion independently correlates with clinical markers of glomerular and tubulointerstitial injury in type 2 diabetic patients[J].Nephrology Dialysis Transplantation,2006,21(12):3428-3434.
[21]Boyle JJ,Weissberg PL,Bennett MR.Tumor necrosis factor-αpromotes macrophage-induced vascular smooth muscle cell apoptosis by direct and autocrine mechanisms[J].Arteriosclerosis,Thrombosis,and Vascular Biology,2003,23(9):1553-1558.
[22]Koike N,Takamura T,Kaneko S.Induction of reactive oxygen species from isolated rat glomeruli by protein kinase C activation and TNF-αstimulation,and effects of a phosphodiesterase inhibitor[J].Life Sciences,2007,80(18):1721-1728.
[23]Mccarthy ET,Sharma R,Sharma M,et al.TNF-αincreases albumin permeability of isolated rat glomeruli through the generation of superoxide[J].Journal of the American Society of Nephrology,1998,9(3):433-438.
[24]Dipetrillo K,Gesek FA.Pentoxifylline ameliorates renal tumor necrosis factor expression,sodium retention,and renal hypertrophy in diabetic rats[J].The American Journal of Nephrology,2004,24(3):352-359.
[25]Schreiner GF,Kohan DE.Regulation of renal transport processes and hemodynamics by macrophages and lymphocytes[J].The American Journal of Physiology-Renal Fluid and Electrolyte Physiology,1990,258(4):761-767.
[26]Mahadevan P,Larkins RG,Fraser JRE,et al.Increased hyaluronan production in the glomeruli from diabetic rats:a link between glucose-induced prostaglandin production and reduced sulphated proteoglycan[J].Diabetologia,1995,38(3):298-305.
[27]Suzuki D,Miyazaki M,Naka R,et al.In situ hybridization of interleukin 6 in diabetic nephropathy[J].Diabetes,1995,44(10):1233-1238.
[28]Dalla Vestra M,Mussap M,Gallina P,et al.Acute-phase markers of inflammation and glomerular structure in patients with type2 diabetes[J].The Journal of the American Society of Nephrology,2005,supplement 1:S78-S82.
[29]Schwarz M,Wahl M,Resch K,et al.IFNγinduces functional chemokine receptor expression in human mesangial cells[J].Clinical&Experimental Immunology,2002,128(2):285-294.
[30]Dai SM,Matsuno H,Nakamura H,et al.Interleukin-18 enhances monocyte tumor necrosis factorαand interleukin-1βproduction induced by direct contact with T lymphocytes:implications in rheumatoid arthritis[J].Arthritis and Rheumatism,2004,50(2):432-443.
[31]Wong CK,Ho AWY,Tong PCY.Aberrant activation profile of cytokines and mitogen-activated protein kinases in type 2 diabetic patients with nephropathy[J].Clinical&Experimental Immunology,2007,149(1):123-131.
[32]Fantuzzi G,Reed DA,Dinarello CA.IL-12-induced IFN gamma is dependent on caspase-1 processing of the IL-18 precursor[J].The Journal of Clinical Investigation,1999,104(6):761-767.
[33]Miyauchi K,Takiyama Y,Honjyo J,et al.Upregulated IL-18expression in type 2 diabetic subjects with nephropathy:TGF-beta1 enhanced IL-18 expression in human renal proximal tubular epithelial cells[J].Diabetes Research and Clinical Practice,2009,83(2):190-199.
[34]Shahzad K,Bock F,Dong W,et al.Nlrp3-inflammasome activation in non-myeloid-derived cells aggravates diabetic nephropathy[J].Kidney International,2015,87(1):74-84.
[2]Atkins RC.The epidemiology of chronic kidney disease[J].Kidney Int Suppl,2005,(94):S14-18.
[3]Martini S,Eichinger F,Nair V,et al.Defining human diabetic nephropathy on the molecular level:integration of transcriptomic profiles with biological knowledge[J].Rev Endocr Metab Disord,2008,9(4):267-2674.
[4]Wada J,Makino H.Inflammation and the pathogenesis of diabetic nephropathy[J].Clin Sci(Lond),2013,124(3):139-152.
[5]Lim AKH,Ma FY,Nikolic-Paterson DJ,et al.Lymphocytes promote albuminuria,but not renal dysfunction or histological damage in a mouse model of diabetic renal injury[J].Diabetologia,2010,53(8):1772-1782.
[6]Awad AS,Kinsey GR,Khutsishvili K,et al.Monocyte/macrophage chemokine receptor CCR2 mediates diabetic renal injury[J].Am J Physiol Renal Physiol,2011,301(6):F1358-1366.
[7]Navarro-Gonzalez JF,Mora-Fernandez C.The role of inflammatory cytokines in diabetic nephropathy[J].Journal of the American Society of Nephrology,2008,19(3):433-442.
[8]Mora C,Navarro JF.Inflammation and diabetic nephropathy[J].Curr Diab Rep,2006,6(6):463-468.
[9]Galkina E and Ley K.Leukocyte recruitment and vascular injury in diabetic nephropathy[J].Journal of the American Society of Nephrology,2006,17(2):368-377.
[10]Aldhahi W,Hamdy O.Adipokines,inflammation,and the endotheliumindiabetes[J].Current Diabetes Reports,2003,3(4):293-298.
[11]Pickup JC.Inflammation and activated innate immunity in the pathogenesis of type 2 diabetes[J].Diabetes Care,2004,27(3):813-823.
[12]Navarro JF,C.Mora C.Role of inflammation in diabetic complications[J].Nephrology Dialysis Transplantation,2005,20(12):2601-2604.
[13]Pickup JC,Chusney GD,Thomas SM,et al.Plasma interleukin-6,tumour necrosis factorαand blood cytokine production in type2 diabetes[J].Life Sciences,2000,67(3):291-300.
[14]Bruno G,Merletti F,Biggeri A,et al.Progression to overt nephropathy in type 2 diabetes:the casale monferrato study[J].Diabetes Care,2003,26(7):2150-2155.
[15]Spranger J,Kroke A,Mohlig M,et al.Inflammatory cytokines and the risk to develop type 2 diabetes:results of the prospective population-based European Prospective Investigation into Cancer and Nutrition(EPIC)-Potsdam Study[J].Diabetes,52(3):812-817.
[16]Hasegawa G,Nakano K,Sawada M,et al.Possible role of tumor necrosis factor and interleukin-1 in the development of diabetic nephropathy[J].Kidney International,1991,40(6):1007-1012.
[17]Navarro JF,Mora C,Macia M,et al.Inflammatory parameters are independently associated with urinary albumin in type 2 diabetes mellitus[J].The American Journal of Kidney Diseases,42(1):53-61.
[18]Dong X,Swaminathan S,Bachman LA,et al.Resident dendritic cells are the predominant TNF-secreting cell in early renal ischemiareperfusion injury[J].Kidney International,71(7):619-628.
[19]Navarro JF,Milena FJ,Mora C,et al.Renal pro-inflammatory cytokine gene expression in diabetic nephropathy:effect of angiotensin-converting enzyme inhibition and pentoxifylline administration[J].The American Journal of Nephrology,2007,26(6):562-570.
[20]Navarro JF,Mora C,Muros M,et al.Urinary tumour necrosis factor-alpha excretion independently correlates with clinical markers of glomerular and tubulointerstitial injury in type 2 diabetic patients[J].Nephrology Dialysis Transplantation,2006,21(12):3428-3434.
[21]Boyle JJ,Weissberg PL,Bennett MR.Tumor necrosis factor-αpromotes macrophage-induced vascular smooth muscle cell apoptosis by direct and autocrine mechanisms[J].Arteriosclerosis,Thrombosis,and Vascular Biology,2003,23(9):1553-1558.
[22]Koike N,Takamura T,Kaneko S.Induction of reactive oxygen species from isolated rat glomeruli by protein kinase C activation and TNF-αstimulation,and effects of a phosphodiesterase inhibitor[J].Life Sciences,2007,80(18):1721-1728.
[23]Mccarthy ET,Sharma R,Sharma M,et al.TNF-αincreases albumin permeability of isolated rat glomeruli through the generation of superoxide[J].Journal of the American Society of Nephrology,1998,9(3):433-438.
[24]Dipetrillo K,Gesek FA.Pentoxifylline ameliorates renal tumor necrosis factor expression,sodium retention,and renal hypertrophy in diabetic rats[J].The American Journal of Nephrology,2004,24(3):352-359.
[25]Schreiner GF,Kohan DE.Regulation of renal transport processes and hemodynamics by macrophages and lymphocytes[J].The American Journal of Physiology-Renal Fluid and Electrolyte Physiology,1990,258(4):761-767.
[26]Mahadevan P,Larkins RG,Fraser JRE,et al.Increased hyaluronan production in the glomeruli from diabetic rats:a link between glucose-induced prostaglandin production and reduced sulphated proteoglycan[J].Diabetologia,1995,38(3):298-305.
[27]Suzuki D,Miyazaki M,Naka R,et al.In situ hybridization of interleukin 6 in diabetic nephropathy[J].Diabetes,1995,44(10):1233-1238.
[28]Dalla Vestra M,Mussap M,Gallina P,et al.Acute-phase markers of inflammation and glomerular structure in patients with type2 diabetes[J].The Journal of the American Society of Nephrology,2005,supplement 1:S78-S82.
[29]Schwarz M,Wahl M,Resch K,et al.IFNγinduces functional chemokine receptor expression in human mesangial cells[J].Clinical&Experimental Immunology,2002,128(2):285-294.
[30]Dai SM,Matsuno H,Nakamura H,et al.Interleukin-18 enhances monocyte tumor necrosis factorαand interleukin-1βproduction induced by direct contact with T lymphocytes:implications in rheumatoid arthritis[J].Arthritis and Rheumatism,2004,50(2):432-443.
[31]Wong CK,Ho AWY,Tong PCY.Aberrant activation profile of cytokines and mitogen-activated protein kinases in type 2 diabetic patients with nephropathy[J].Clinical&Experimental Immunology,2007,149(1):123-131.
[32]Fantuzzi G,Reed DA,Dinarello CA.IL-12-induced IFN gamma is dependent on caspase-1 processing of the IL-18 precursor[J].The Journal of Clinical Investigation,1999,104(6):761-767.
[33]Miyauchi K,Takiyama Y,Honjyo J,et al.Upregulated IL-18expression in type 2 diabetic subjects with nephropathy:TGF-beta1 enhanced IL-18 expression in human renal proximal tubular epithelial cells[J].Diabetes Research and Clinical Practice,2009,83(2):190-199.
[34]Shahzad K,Bock F,Dong W,et al.Nlrp3-inflammasome activation in non-myeloid-derived cells aggravates diabetic nephropathy[J].Kidney International,2015,87(1):74-84.