Chronic obstructive pulmonary disease induced by exposure to biomass smoke is associated with a Th2 cytokine production profile

被引:43
作者
Solleiro-Villavicencio, Helena [1 ]
Quintana-Carrillo, Roger [2 ]
Falfan-Valencia, Ramces [3 ]
Ines Vargas-Rojas, Maria [1 ,4 ]
机构
[1] Univ Nacl Autonoma Mexico, Fac Med, Programa Doctorado Ciencias Biomed, Mexico City 04510, DF, Mexico
[2] Inst Nacl Salud Publ, Dept Invest Tabaco, Cuernavaca, Morelos, Mexico
[3] Inst Natl Enfermedades Resp Ismael Cosio Villegas, Lab HLA, Mexico City, DF, Mexico
[4] Inst Natl Enfermedades Resp Ismael Cosio Villegas, Dept Invest Microbiol, Mexico City, DF, Mexico
关键词
COPD; Cigarette smoke; Biomass smoke; Cytokines; T helper cells; T-CELLS; COPD; EXPRESSION; IL-17;
D O I
10.1016/j.clim.2015.07.009
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
Smoking and exposure to biomass smoke induce the release of pro-inflammatory mediators and the activation of T helper cells. The resulting inflammatory response contributes to the development of COPD. Clinical heterogeneity exists among COPD patients, particularly between patients with disease associated with tobacco smoking (TS-COPD) and those exposed to biomass smoke (BE-COPD). The aim of this study was to identify whether exposure to tobacco and biomass smokes promotes different Th responses that contribute to clinical variability. The study only included women. The frequency of Th17 cells in patients with TS-COPD was significantly higher than in patients with BE-COPD and healthy controls (HC). In contrast, patients with BE-COPD had higher levels of Th2 cells than TS-COPD and HC. In accordance, IL-4 serum concentration was higher in BE-COPD than in TS-COPD. Our data indicates that the different responses induced by these two irritants may underlie the clinical heterogeneity between TS- and BE-COPD patients. (C) 2015 Elsevier Inc. All rights reserved.
引用
收藏
页码:150 / 155
页数:6
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