Women with COPD from biomass smoke have reduced serum levels of biomarkers of angiogenesis and cancer, with EGFR predominating, compared to women with COPD from smoking

Abstract

The main causes of COPD are smoking (COPD-TS) and exposure to biomass smoke (COPD-BS), considered as different phenotypes. The association of COPD-TS with lung cancer (LC) is well established, but not in COPD-BS. Thus, we studied the serum concentration of cytokines that participate in inflammation, angiogenesis, and tumor progression, used frequently as LC biomarkers, in women with COPD-BS compared with COPD-TS (n = 70). Clinical and physiological characteristics and the serum concentration (multiplex immunoassay) of 16 cytokines were evaluated. The analysis revealed that women with COPD-BS were shorter and older, and had lower concentrations of 12 serum cytokines: 6 proinflammatory and angiogenic IL-6Rα, PECAM-1, leptin, osteopontin, prolactin, and follistatin; and 6 that participate in angiogenesis and in tumor progression FGF-2, HGF, sVEGFR-2, sHER2/neu, sTIE-2, G-CSF, and SCF. Notably, there was a significant increase in sEGFR in women with COPD-BS compared to women with COPD-TS. PDGF-AA/BB and sTIE-2 did not change. These findings suggest that women with COPD-BS have markedly decreased proinflammatory, angiogenic, and tumor progression potential, compared to women with COPD-TS, with sEGFR as the predominant mediator, which might reflect a differential pattern of inflammation in women exposed to BS, favoring the development of chronic bronchitis.