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The Proceedings of the American Thoracic Society 3:475-476 (2006)
© 2006 The American Thoracic Society
doi: 10.1513/pats.200603-038MS
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Interleukin-6 Gene Polymorphism Confers Susceptibility to Pulmonary Hypertension in Chronic Obstructive Pulmonary Disease

Saadia Eddahibi, Ari Chaouat, Li Tu, Christos Chouaid, Emmanuel Weitzenblum, Bruno Housset, Bernard Maitre and Serge Adnot

INSERM U492 and Département de Physiologie, Hôpital H. Mondor; Service de Pneumologie, Hôpital Intercommunal de Créteil, Créteil; and Service de Pneumologie, Hôpital de Hautepierre, Strasbourg, France

Correspondence and requests for reprints should be addressed to Serge Adnot, M.D., Professeur de Physiologie, Service de Physiologie–Explorations Fonctionnelles, Hôpital Henri Mondor, 94010 Creteil, France. E-mail: serge.adnot{at}creteil.inserm.fr

Because of its high prevalence, chronic obstructive pulmonary disease (COPD) is the most frequent cause of precapillary pulmonary hypertension (PH) due to chronic hypoxic lung disease (1). PH associated with COPD is usually mild to moderate, with a resting pulmonary artery mean pressure ranging between 20 and 35 mm Hg. However, it may increase markedly during sleep, exercise, and exacerbation of the respiratory failure. Moreover, the level of pulmonary artery pressure is a good indicator of prognosis in patients with COPD. The pathogenesis of PH in patients with advanced COPD is incompletely understood. Chronic hypoxemia, morphologic changes in lung parenchyma (2, 3), and inflammation (4) are potential contributing factors. Here, we investigated whether inflammatory cytokines were related to the PH process in COPD. In 50 patients with COPD (age, 62 ± 3 yr), pulmonary artery pressure (Pap) was measured during right heart catheterization, and blood samples were collected for determination of genotypes and serum levels of interleukin (IL)-1ß, IL-6, and monocyte chemoattractant protein-1 (MCP-1). As compared with a control group of 50 smokers, patients with COPD had elevated serum levels of IL-6 (p < 0.001) and MCP-1 (p < 0.01) but unchanged levels of IL-1ß. Pap was positively correlated with serum IL-6 levels but not with serum IL-1ß and MCP-1 levels. The IL-6 G/G polymorphism (–174G/C) correlated with a higher level of IL-6 among patients with COPD but not among control subjects. Patients carrying the IL6 GG genotype showed higher serum levels of IL-6 and higher Pap than those carrying the CC or CG genotype. These results indicate that the inflammatory cytokine IL-6 may contribute to PH in COPD and that IL-6 gene polymorphism confers susceptibility to PH in patients with COPD. Since we previously reported that the serotonin transporter (5-HTT) gene polymorphism was associated with PH in COPD, the combined actions of the allelic variants of these two genes are being examined in a larger population of patients with COPD.

FOOTNOTES

Conflict of Interest Statement: None of the authors has a financial relationship with a commercial entity that has an interest in the subject of this manuscript.

(Received in original form March 16, 2006; accepted in final form March 21, 2006)

REFERENCES

  1. Pauwels RA, Rabe KF. Burden and clinical features of chronic obstructive pulmonary disease (COPD). Lancet 2004;364:613–620.[CrossRef][Medline]
  2. Eddahibi S, Fabre V, Boni C, Martres MP, Raffestin B, Hamon M, Adnot S. Induction of serotonin transporter by hypoxia in pulmonary vascular smooth muscle cells. Relationship with the mitogenic action of serotonin. Circ Res 1999;84:329–336.[Abstract/Free Full Text]
  3. Eddahibi S, Chaouat A, Morrell N, Fadel E, Fuhrman C, Bugnet AS, Dartevelle P, Housset B, Hamon M, Weitzenblum E, et al. Polymorphism of the serotonin transporter gene and pulmonary hypertension in chronic obstructive pulmonary disease. Circulation 2003;108:1839–1844.[Abstract/Free Full Text]
  4. Humbert M, Monti G, Brenot F, Sitbon O, Portier A, Grangeot-Keros L, Duroux P, Galanaud P, Simonneau G, Emilie D. Increased interleukin-1 and interleukin-6 serum concentrations in severe primary pulmonary hypertension. Am J Respir Crit Care Med 1995;151:1628–1631.[Abstract]




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