Macrophage phenotype and its relationship with renal function in human diabetic nephropathy
Autoři:
Xiaoliang Zhang aff001; Ying Yang aff001; Yu Zhao aff001
Působiště autorů:
Institute of Nephrology, Zhong Da Hospital, Southeast University, School of Medicine, Nanjing, Jiangsu, China
aff001
Vyšlo v časopise:
PLoS ONE 14(9)
Kategorie:
Research Article
doi:
https://doi.org/10.1371/journal.pone.0221991
Souhrn
This study aimed to examine the macrophage phenotype and its relationship to renal function and histological changes in human DN and the effect of TREM-1 on high-glucose-induced macrophage activation. We observed that in renal tissue biopsies, the expression of CD68 and M1 was apparent in the glomeruli and interstitium, while accumulation of M2 and TREM-1 was primarily observed in the interstitium. The numbers of CD68, M1, and M2 macrophages infiltrating in the DN group were increased in a process-dependent manner compared with the control group, and the intensities of the infiltrates were proportional to the rate of subsequent decline in renal function. M1 macrophages were recruited into the kidney at an early stage (I+IIa) of DN. The M1-to-M2 macrophage ratio peaked at this time, whereas M2 macrophages predominated at later time points (III) when the percentage of M1/M2 macrophages was at its lowest level. In an in vitro study, we showed that under high glucose conditions, macrophages began to up-regulate their expression of TREM-1, M1, and marker iNOS and decreased the M2 marker MR. However, the above effects of high-glucose were abolished when TREM-1 expression was inhibited by TREM-1 siRNA. In conclusion, our study demonstrated that there was a positive correlation between the M1/M2 activation state and the progress of DN, and TREM-1 played an important role in high-glucose-induced macrophage phenotype transformation.
Klíčová slova:
Biology and life sciences – Cell biology – Cellular types – Animal cells – Blood cells – White blood cells – Macrophages – Immune cells – Genetics – Gene expression – Gene regulation – Small interfering RNAs – Phenotypes – Biochemistry – Nucleic acids – RNA – Non-coding RNA – Anatomy – Renal system – Kidneys – Physiology – Developmental biology – Molecular development – Medicine and health sciences – Immunology – Immune system – Innate immune system – Cytokines – Endocrinology – Endocrine disorders – Metabolic disorders – Immune physiology – Physical sciences – Chemistry – Chemical compounds – Organic compounds – Carbohydrates – Monosaccharides – Glucose – Organic chemistry
Zdroje
1. Shaw J.E., Sicree R.A. and Zimmet P.Z. Global estimates of the prevalence of diabetes for 2010 and 2030. Diabetes Res Clin Pract, 2010, 87: 4–14. doi: 10.1016/j.diabres.2009.10.007 19896746
2. Domingueti C.P., Dusse L.M., Carvalho M., de Sousa L.P., Gomes K.B. and Fernandes A.P. Diabetes mellitus: The linkage between oxidative stress, inflammation, hypercoagulability and vascular complications. J Diabetes Complications, 2016, 30: 738–45. doi: 10.1016/j.jdiacomp.2015.12.018 26781070
3. Navarro-Gonzalez J.F. and Mora-Fernandez C. The role of inflammatory cytokines in diabetic nephropathy. J Am Soc Nephrol, 2008, 19: 433–42. doi: 10.1681/ASN.2007091048 18256353
4. Tesch G.H. Role of macrophages in complications of type 2 diabetes. Clin Exp Pharmacol Physiol, 2007, 34: 1016–9. doi: 10.1111/j.1440-1681.2007.04729.x 17714088
5. Wang Y., Wang Y., Cao Q., Zheng G., Lee V.W., Zheng D., et al. By homing to the kidney, activated macrophages potently exacerbate renal injury. Am J Pathol, 2008, 172: 1491–9. doi: 10.2353/ajpath.2008.070825 18467704
6. Wang N., Liang H. and Zen K. Molecular mechanisms that influence the macrophage m1-m2 polarization balance. Front Immunol, 2014, 5: 614. doi: 10.3389/fimmu.2014.00614 25506346
7. Gordon S. and Taylor P.R. Monocyte and macrophage heterogeneity. Nat Rev Immunol, 2005, 5: 953–64. doi: 10.1038/nri1733 16322748
8. Sica A. and Mantovani A. Macrophage plasticity and polarization: in vivo veritas. J Clin Invest, 2012, 122: 787–95. doi: 10.1172/JCI59643 22378047
9. Ricardo S.D., van Goor H. and Eddy A.A. Macrophage diversity in renal injury and repair. J Clin Invest, 2008, 118: 3522–30. doi: 10.1172/JCI36150 18982158
10. Erwig L.P., Kluth D.C. and Rees A.J. Macrophage heterogeneity in renal inflammation. Nephrol Dial Transplant, 2003, 18: 1962–5. doi: 10.1093/ndt/gfg313 13679464
11. Ford J.W. and McVicar D.W. TREM and TREM-like receptors in inflammation and disease. Curr Opin Immunol, 2009, 21: 38–46. doi: 10.1016/j.coi.2009.01.009 19230638
12. Ornatowska M., Azim A.C., Wang X., Christman J.W., Xiao L., Joo M., et al. Functional genomics of silencing TREM-1 on TLR4 signaling in macrophages. Am J Physiol Lung Cell Mol Physiol, 2007, 293: L1377–84. doi: 10.1152/ajplung.00140.2007 17905855
13. Klesney-Tait J., Turnbull I.R. and Colonna M. The TREM receptor family and signal integration. Nat Immunol, 2006, 7: 1266–73. doi: 10.1038/ni1411 17110943
14. Lo T.H., Tseng K.Y., Tsao W.S., Yang C.Y., Hsieh S.L., Chiu A.W., et al. TREM-1 regulates macrophage polarization in ureteral obstruction. Kidney Int, 2014, 86: 1174–86. doi: 10.1038/ki.2014.205 24918157
15. Tervaert T.W., Mooyaart A.L., Amann K., Cohen A.H., Cook H.T., Drachenberg C.B., et al. Pathologic classification of diabetic nephropathy. J Am Soc Nephrol, 2010, 21: 556–63. doi: 10.1681/ASN.2010010010 20167701
16. Turgut F. and Bolton W.K. Potential new therapeutic agents for diabetic kidney disease. Am J Kidney Dis, 2010, 55: 928–40. doi: 10.1053/j.ajkd.2009.11.021 20138415
17. Downs C.A. and Faulkner M.S. Toxic stress, inflammation and symptomatology of chronic complications in diabetes. World J Diabetes, 2015, 6: 554–65. doi: 10.4239/wjd.v6.i4.554 25987953
18. Wada J. and Makino H. Inflammation and the pathogenesis of diabetic nephropathy. Clin Sci (Lond), 2013, 124: 139–52.
19. Wilson H.M., Walbaum D. and Rees A.J. Macrophages and the kidney. Curr Opin Nephrol Hypertens, 2004, 13: 285–90. 15073486
20. Chow F., Ozols E., Nikolic-Paterson D.J., Atkins R.C. and Tesch G.H. Macrophages in mouse type 2 diabetic nephropathy: correlation with diabetic state and progressive renal injury. Kidney Int, 2004, 65: 116–28. doi: 10.1111/j.1523-1755.2004.00367.x 14675042
21. Lim A.K. and Tesch G.H. Inflammation in diabetic nephropathy. Mediators Inflamm, 2012, 2012: 146154. doi: 10.1155/2012/146154 22969168
22. Coimbra T.M., Janssen U., Grone H.J., Ostendorf T., Kunter U., Schmidt H., et al. Early events leading to renal injury in obese Zucker (fatty) rats with type II diabetes. Kidney Int, 2000, 57: 167–82. doi: 10.1046/j.1523-1755.2000.00836.x 10620198
23. Alikhan M.A. and Ricardo S.D. Mononuclear phagocyte system in kidney disease and repair. Nephrology (Carlton), 2013, 18: 81–91.
24. Mantovani A., Biswas S.K., Galdiero M.R., Sica A. and Locati M. Macrophage plasticity and polarization in tissue repair and remodelling. J Pathol, 2013, 229: 176–85. doi: 10.1002/path.4133 23096265
25. Mege J.L., Mehraj V. and Capo C. Macrophage polarization and bacterial infections. Curr Opin Infect Dis, 2011, 24: 230–4. doi: 10.1097/QCO.0b013e328344b73e 21311324
26. Wang Y., Wang Y.P., Zheng G., Lee V.W., Ouyang L., Chang D.H., et al. Ex vivo programmed macrophages ameliorate experimental chronic inflammatory renal disease. Kidney Int, 2007, 72: 290–9. doi: 10.1038/sj.ki.5002275 17440493
27. Kluth D.C. Pro-resolution properties of macrophages in renal injury. Kidney Int, 2007, 72: 234–6. doi: 10.1038/sj.ki.5002332 17653230
28. Lee S., Huen S., Nishio H., Nishio S., Lee H.K., Choi B.S., et al. Distinct macrophage phenotypes contribute to kidney injury and repair. J Am Soc Nephrol, 2011, 22: 317–26. doi: 10.1681/ASN.2009060615 21289217
29. Han Y., Ma F.Y., Tesch G.H., Manthey C.L. and Nikolic-Paterson D.J. Role of macrophages in the fibrotic phase of rat crescentic glomerulonephritis. Am J Physiol Renal Physiol, 2013, 304: F1043–53. doi: 10.1152/ajprenal.00389.2012 23408165
30. Zhang X.L., Guo Y.F., Song Z.X. and Zhou M. Vitamin D prevents podocyte injury via regulation of macrophage M1/M2 phenotype in diabetic nephropathy rats. Endocrinology, 2014, 155: 4939–50. doi: 10.1210/en.2014-1020 25188527
31. Zhang X., Zhou M., Guo Y., Song Z. and Liu B. 1,25-Dihydroxyvitamin D(3) Promotes High Glucose-Induced M1 Macrophage Switching to M2 via the VDR-PPARgamma Signaling Pathway. Biomed Res Int, 2015, 2015: 157834. doi: 10.1155/2015/157834 25961000
32. Anders H.J. and Ryu M. Renal microenvironments and macrophage phenotypes determine progression or resolution of renal inflammation and fibrosis. Kidney Int, 2011, 80: 915–925. doi: 10.1038/ki.2011.217 21814171
33. Tesch G.H. Macrophages and diabetic nephropathy. Semin Nephrol, 2010, 30: 290–301. doi: 10.1016/j.semnephrol.2010.03.007 20620673
34. Wang Y. and Harris D.C. Macrophages in renal disease. J Am Soc Nephrol, 2011, 22: 21–7. doi: 10.1681/ASN.2010030269 21209251
35. Bouchon A., Dietrich J. and Colonna M. Cutting edge: inflammatory responses can be triggered by TREM-1, a novel receptor expressed on neutrophils and monocytes. J Immunol, 2000, 164: 4991–5. doi: 10.4049/jimmunol.164.10.4991 10799849
36. Schenk M., Bouchon A., Birrer S., Colonna M. and Mueller C. Macrophages expressing triggering receptor expressed on myeloid cells-1 are underrepresented in the human intestine. J Immunol, 2005, 174: 517–24. doi: 10.4049/jimmunol.174.1.517 15611278
37. Radsak M.P., Salih H.R., Rammensee H.G. and Schild H. Triggering receptor expressed on myeloid cells-1 in neutrophil inflammatory responses: differential regulation of activation and survival. J Immunol, 2004, 172: 4956–63. doi: 10.4049/jimmunol.172.8.4956 15067076
38. Colonna M. and Facchetti F. TREM-1 (triggering receptor expressed on myeloid cells): a new player in acute inflammatory responses. J Infect Dis, 2003, 187 Suppl 2: S397–401.
39. Wu J., Li J., Salcedo R., Mivechi N.F., Trinchieri G. and Horuzsko A. The proinflammatory myeloid cell receptor TREM-1 controls Kupffer cell activation and development of hepatocellular carcinoma. Cancer Res, 2012, 72: 3977–86. doi: 10.1158/0008-5472.CAN-12-0938 22719066
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