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Article

Clare M. Lloyd^*,,¶, Andrew W. Minto^*, Martin E. Dorf, Amanda Proudfoot^||, Timothy N.C. Wells^||, David J. Salant^*, and Jose-Carlos Gutierrez-Ramos^,¶

From the ^* Department of Medicine, Boston University Medical Center, Boston, Massachusetts 02118; The Center for Blood Research, Incorporated and Department of Genetics and the Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115; ^|| Glaxo Institute for Molecular Biology, Geneva, CH1228 Switzerland; and ^¶ Millennium Pharmaceuticals Inc., Cambridge Massachusets 02139

The involvement of chemokines in inflammation is well established, but their functional role in disease progression, and particularly in the development of fibrosis, is not yet understood. To investigate the functional role that the chemokines monocyte chemoattractant protein–1 (MCP-1) and RANTES play in inflammation and the progression to fibrosis during crescentic nephritis we have developed and characterized a murine model for this syndrome. Significant increases in T-lymphocytes and macrophages were observed within glomeruli and interstitium, paralleled by an induction of mRNA expression of MCP-1 and RANTES, early after disease initiation. Blocking the function of MCP-1 or RANTES resulted in significant decreases in proteinuria as well as in numbers of infiltrating leukocytes, indicating that both MCP-1 and RANTES (regulated upon activation in normal T cells expressed and secreted) play an important role in the inflammatory phase of crescentic nephritis. In addition, neutralization of MCP-1 resulted in a dramatic decrease in both glomerular crescent formation and deposition of type I collagen. These results highlight a novel role for MCP-1 in crescent formation and development of interstitial fibrosis, and indicate that in addition to recruiting inflammatory cells this chemokine is critically involved in irreversible tissue damage.

The authors are indebted to Drs. Ramzi Cotran and Jose-Angel Gonzalo for helpful discussion while preparing this manuscript.

This work has been funded by National Institutes of Health grants DK30932 (D.J. Salant) and HL 14867502, CiCyT PB93-0317, HL94-10-B and the Aplastic Foundation of America (J.-C. Gutierrez-Ramos). J.-C. Guttierrez-Ramos is the Amy C. Potter Fellow.

¹ Abbreviations used in this paper: CINC, cytokin-induced neutrophil chemoattractant; GN, glomerulonephritis; IP-10, interferon-inducible protein 10 kD; ISH, in situ hybridization; MCP-1, monocyte chemoattractant protein-1; NSS, normal sheep serum; NTS, nephrotoxic serum; RANTES, regulated upon activation in normal T cells expressed and secreted.

This work was presented in part at the 29th Annual Meeting of the American Society of Nephrology, New Orleans, Louisiana.

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