Background Pulmonary artery remodeling triggered by alveolar hypoxia is considered the
main mechanism of pulmonary hypertension (PH) in COPD patients. We hypothesized that
the risk for PH in COPD is increased by an elevation in the proinflammatory cytokines
interleukin (IL)-6, monocyte chemoattractant protein-1 (MCP-1), and IL-1β, as well as by
specific genetic polymorphisms of these cytokines. Methods We assessed cytokine plasma
levels and the polymorphisms G (− 174) C IL-6, C (− 511) T IL-1β, and A (− 2518) G MCP-1 …