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Am. J. Respir. Crit. Care Med., Volume 165, Number 4, February 2002, 534-539

Chemokine RANTES in Severe Pulmonary Arterial Hypertension

PETER DORFMÜLLER, VÉRONIQUE ZARKA, INGRID DURAND-GASSELIN, GIANPAOLA MONTI, KARL BALABANIAN, GILLES GARCIA, FRÉDÉRIQUE CAPRON, AURORE COULOMB-LHERMINÉ, ANNE MARFAING-KOKA, GÉRALD SIMONNEAU, DOMINIQUE EMILIE, and MARC HUMBERT

Center for Pulmonary Vascular Diseases, UPRES EA 2705; Department of Respiratory and Intensive Care Medicine, INSERM U1 3 1; Department of Pathology; and Department of Hematology, South-Paris Cytokine Institute, Antoine Béclère Hospital, Assistance Publique Hôpitaux de Paris, South-Paris University, Clamart, France

The recent discovery that sporadic and familial primary pulmonary hypertension can be associated with germline mutations of genes encoding receptor members of the transforming growth factor-beta family has focused much attention on cytokines and growth factors in pulmonary vascular disorders. Production of several cytokines has been demonstrated in severe pulmonary arterial hypertension, emphasizing the possible influence of inflammatory mechanisms in this condition. Moreover, perivascular inflammatory cell infiltrates composed of macrophages and lymphocytes have been detected in plexiform lesions of primary pulmonary hypertension. Chemokine RANTES is an important chemoattractant for monocytes and T cells. We therefore hypothesize that chemokine RANTES promotes cell recruitment in the lungs of patients displaying severe pulmonary arterial hypertension. Reverse transcriptase polymerase chain reaction demonstrated elevated RANTES mRNA expression in 10 lung samples from patients with severe pulmonary arterial hypertension, as compared with seven control subjects. In situ hybridization and immunohistochemistry confirmed that endothelial cells were the major source of RANTES within the pulmonary artery wall of the patients. Serial sections analysis showed that RANTES expression was associated with CD45+ inflammatory cell infiltrates. These results support the concept that inflammatory mechanisms play a role in the natural history of pulmonary arterial hypertension.




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