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.

COPD 的主要原因是吸烟 (COPD-TS) 和暴露于生物质烟雾 (COPD-BS)，被认为是不同的表型。COPD-TS 与肺癌 (LC) 的相关性已得到充分证实，但在 COPD-BS 中则不然。因此，我们研究了 COPD-BS 女性与 COPD-TS 女性（n = 70）中参与炎症、血管生成和肿瘤进展的细胞因子的血清浓度，这些细胞因子经常用作 LC 生物标志物。评估了 16 种细胞因子的临床和生理特征以及血清浓度（多重免疫测定）。分析显示，患有 COPD-BS 的女性更矮、更年长，12 种血清细胞因子的浓度较低：6 种促炎和血管生成 IL-6Rα、PECAM-1、瘦素、骨桥蛋白、催乳素和卵泡抑素；和 6 参与血管生成和肿瘤进展 FGF-2、HGF、sVEGFR-2，sHER2/neu、sTIE-2、G-CSF 和 SCF。值得注意的是，与患有 COPD-TS 的女性相比，患有 COPD-BS 的女性的 sEGFR 显着增加。PDGF-AA/BB 和 sTIE-2 没有变化。这些发现表明，与 COPD-TS 女性相比，COPD-BS 女性的促炎、血管生成和肿瘤进展潜力显着降低，sEGFR 作为主要介质，这可能反映了暴露于 BS 的女性炎症的不同模式，有利于慢性支气管炎的发展。