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Interleukin-6 Causes Mild Pulmonary Hypertension and Augments Hypoxia-Induced Pulmonary Hypertension in Mice*

Scott M. Golembeski, MS; James West, PhD; Yuji Tada, MD; Karen A. Fagan, MD
Author and Funding Information

*From the University of Colorado Health Sciences Center, Department of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, Center for Genetic Lung Diseases, Cardiovascular Pulmonary Research Laboratory, Denver, CO. This research was supported by AHA-SDG 0230255N (Dr. West) and NIH RO1 HL66328 and AHA-EIA 0340122N (Dr. Fagan).

Correspondence to: Karen Fagan, MD, University of Colorado Health Sciences Center, Department of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, Center for Genetic Lung Diseases, Cardiovascular Pulmonary Research Laboratory, 4200 East Ninth Ave, C#272, Denver, CO 80262; e-mail: karen.fagan@uchsc.edu



Chest. 2005;128(6_suppl):572S-573S. doi:10.1378/chest.128.6_suppl.572S-a
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Inflammation may play a central role in the pathogenesis of pulmonary arterial hypertension (PAH). Levels of interleukin (IL)-6, IL-1, C-reactive protein, regulated on activation normal T cells expressed and secreted (RANTES), and fractalkine are increased in the serum and lungs of PAH patients. Scleroderma, lupus, mixed connective tissue disease, Castleman disease, HIV, and polyneuropathy/organomegaly/endocrinopathy/M protein/skin changes (POEMS syndrome) are associated with increased IL-6 and PAH. IL-6 may play a pathogenic role through inflammation, cellular proliferation, interaction with bone morphogenetic protein pathways, decreasing prostacyclin levels, and induction of the production of other mediators such as serotonin, endothelin (ET)-1 and vascular endothelial growth factor. Experimental models of pulmonary hypertension (PH), including hypoxia and monocrotaline, are associated with increased IL-6 levels. Previous studies have found right ventricular hypertrophy (RVH) in rats treated with recombinant human IL-6. This was associated with evidence of vascular thrombosis and may be a model of chronic thromboembolic PAH. We hypothesized that IL-6 would cause PH in mice and that IL-6 may potentiate the development of PH following chronic hypoxia in mice.

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