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a Department of Internal Medicine and Geriatrics, University Hospital, Montpellier, France
b Laboratory of Biology in Nutrition, Nancy-Brabois University Hospital, Vandoeuvre-lès-Nancy, France
c Department of Histology, Nancy-Brabois University Hospital, Vandoeuvre-lès-Nancy, France
d Department of Internal Medicine and Geriatrics, René Muret-Bigottini Hospital, Sevran, France
Claude Jeandel, Service de Médecine Interne-Gériatrie, Centre de Prévention et de Traitement des Maladies du Vieillissement, 39 Avenue Charles Flahault, 34295 Montpellier Cedex 5, France E-mail: c-jeandel{at}chu-montpellier.fr.
Background. Giant cell arteritis (GCA) is a subacute periarteritis predominantly affecting segments of the external carotids of elderly patients. Vasculitic lesions in GCA samples might be characterized by in situ production of cytokines mRNA, indicative of macrophage and T-cell activation. However, whether the cytokine production of vessels with arteritis differs from that of vessels exposed to inflammatory conditions that originate peripheral to the vessel remains unknown.
Methods. We investigated cytokine and soluble receptor cytokine production in blood samples and cultures of human temporal arteries from 22 consecutive patients (mean age 77 ± 6 years) further investigated for possible diagnosis of GCA: 7 patients had GCA and 15 had neither GCA nor vasculitis but had other inflammatory, infectious, or malignant diseases (controls). The production of cytokines and soluble cytokine receptors in the supernatants of cultures of 3-mm segments of temporal artery specimens, before and after lipopolysaccharide (LPS) stimulation (10 ng/ml and 10 µg/ml) and in serum, was quantified using sandwich enzyme-linked immunosorbent assay (ELISA).
Results. Cytokine production by temporal arteries increased significantly and in a dose-dependent manner (p < .01) after LPS stimulation in all patients studied, suggesting that the system is methodologically functional. Despite a large interindividual variation, we found similar differences in cytokine production before and after stimulation by 10 ng/ml and 10 µg/ml LPS between both groups: temporal arteries of GCA patients produced more interleukin (IL)-1ß (p < .05) and IFN
(nonsignificant) and less tumor necrosis factor (TNF)
(p < .05) and IL-6 (nonsignificant) than temporal arteries of controls. The levels of TNF (p < .05) and IL-6 soluble receptor (p < .05) were significantly lower in GCA patients as compared with controls in blood samples, whereas levels of cytokines in temporal artery and in blood samples were not significantly correlated at the individual level in both groups.
Conclusions. The present pilot study, which requires further confirmation on a larger number of well-defined patients with GCA, suggests that a specific arterial cytokine production profile might exist in GCA (high IL-1ß ± IFN and low TNF), addresses the question of the mechanisms by which IL-1ß and TNF might be differentially regulated at the level of the arterial cell wall, and supports the view that cultures of the temporal artery might be an interesting tool for evaluating the role of cytokines in GCA pathogenesis.
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  C. M. Weyand and J. J. Goronzy Medium- and Large-Vessel Vasculitis N. Engl. J. Med., July 10, 2003; 349(2): 160 - 169. [Full Text] [PDF]
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