Rheumatology Advance Access originally published online on April 18, 2006
Rheumatology 2006 45(11):1356-1363; doi:10.1093/rheumatology/kel128
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Association between increased CCL2 (MCP-1) expression in lesions and persistence of disease activity in giant-cell arteritis*
1Department of Internal Medicine and 2Department of Pathology, Hospital Clínic, Vasculitis Research Unit, University of Barcelona, Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain and 3Craniofacial Developmental Biology and Regeneration Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda MD, USA.
Correspondence to: Maria C. Cid, MD, Department of Internal Medicine, Hospital Clínic, Villarroel 170, Barcelona 08036, Spain. E-mail: mccid{at}clinic.ub.es
Objective. Patients with giant-cell arteritis (GCA) usually respond dramatically to corticosteroid treatment. However, recurrences are frequent and corticosteroid requirements are highly variable among patients. The aim of our study was to identify genes potentially involved in disease persistence.
Methods. Gene expression was explored with cDNA arrays in temporal artery biopsies from six GCA patients with relapsing disease and six patients who easily achieved sustained remission. Differentially expressed genes of interest were subsequently analysed by quantitative real-time polymerase chain reaction (PCR) and immunohistochemistry in temporal artery biopsies from 35 patients with biopsy-proven GCA and nine controls.
Results. CCL2 (MCP-1) was up-regulated in temporal artery samples from relapsing individuals. In the extended series of patients, CCL2 mRNA concentration in lesions was significantly higher than in controls (31 ± 15.6 vs 0.44 ± 0.10, P = 0.0001). In addition, CCL2 was more abundant in patients who experienced two or more relapses during the first year compared with those who endured sustained remission (127 ± 82 vs 11 ± 5.5, P = 0.0233) and correlated with the cumulated prednisolone dose (R = 0.533, P = 0.0024). CCL2 mRNA concentration correlated with IL-1ß (R = 0.45, P = 0.02), tumour necrosis factor-
(TNF-) (R = 0.47, P = 0.013) and IL-6 (R = 0.52, P = 0.0053) mRNA. However, circulating CCL2 determined by ELISA was decreased in patients with strong systemic inflammatory response, suggesting that reduction in circulating CCL2 may reinforce the local gradient in lesions.
Conclusion. Increased CCL2 (MCP-1) expression in lesions is associated with persistence of disease activity in GCA.
KEY WORDS: Vasculitis, Inflammation, Chemokines
* Results presented at the 12th International Vasculitis and ANCA Workshop. Heidelberg, Germany, June 2005 and at the Annual Scientific meeting of the American College of Rheumatology, San Diego, CA, USA, November 2005.
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