Lung Damage among Individuals with Biomass Smoke Exposure Characterized by CT Features and Changes in Pulmonary Function

Abstract BackgroundBiomass smoke exposure (BSE) is an important etiological factor in chronic obstructive pulmonary disease (COPD). However, few studies have focused on the effects of BSE in the respiratory muscles or lungs.MethodsUsing a cohort, we selected 98 participants in underdeveloped rural areas: 16 healthy individuals with BSE (“BSE normal”), 19 patients with BSE and COPD (“BSE+COPD”), 13 healthy individuals with cigarette smoke exposure (“CSE normal”), 25 patients with cigarette smoke exposure and COPD (“CSE+COPD”), and 25 healthy controls. Patients with GOLD stage I and II COPD were included. Baseline data (demographic data, BSE or CSE, lung function, and CT findings) and follow-up lung function data were collected. CT parameters of emphysema, pulmonary small vessels, airway remodeling, pectoralis muscles, and erector spinae muscle were measured.ResultsIndividuals with BSE were mainly women (32/35, 91.43%). Compared with the CSE+COPD group, the BSE+COPD group demonstrated slow lung function decline, increased lower lung emphysema, and narrower airway lumen and airway wall thickening in moderate and small airways (all P<.05). Compared with healthy controls, the CSE normal and BSE normal groups exhibited significant reduction of pulmonary small vessel area and obvious airway remodeling in small airways (P<.05). Compared with the BSE normal group, the BSE+COPD group showed significantly more severe emphysema and airway remodeling, as well as reduced left pectoralis major muscle area (all P<.05).ConclusionsHealthy individuals with BSE had reduced pulmonary small vessel area and obvious airway remodeling; patients with BSE and COPD showed more severe emphysema, airway remodeling, and pectoralis major muscle change. More investigations are needed regarding interventions for BSE.Trial registration: ChiCTR, ChiCTR-OO-14004264 . Registered 12 February 2014, http://www.chictr.org.cn/showproj.aspx?proj=5304

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Reduced lung function due to biomass smoke exposure in young adults in rural Nepal

European Respiratory Journal ◽

10.1183/09031936.00220511 ◽

2012 ◽

Vol 41 (1) ◽

pp. 25-30 ◽

Cited By ~ 41

Author(s):

O. P. Kurmi ◽

G. S. Devereux ◽

W. C. S. Smith ◽

S. Semple ◽

M. F. C. Steiner ◽

...

Keyword(s):

Young Adults ◽

Lung Function ◽

Smoke Exposure ◽

Biomass Smoke ◽

Biomass Smoke Exposure ◽

Rural Nepal

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Macrophages Inhibit Ciliary Protein Levels by Secreting BMP-2 Leading to Airway Epithelial Remodeling Under Cigarette Smoke Exposure

Frontiers in Molecular Biosciences ◽

10.3389/fmolb.2021.663987 ◽

2021 ◽

Vol 8 ◽

Author(s):

Zhigang Wang ◽

Wenzhang Liang ◽

Cuiqing Ma ◽

Jiachao Wang ◽

Xue Gao ◽

...

Keyword(s):

Cigarette Smoke ◽

Airway Epithelium ◽

Airway Remodeling ◽

Inhibitory Effect ◽

Smoke Exposure ◽

Cigarette Smoke Exposure ◽

Protein Levels ◽

Ciliary Protein ◽

Β Tubulin ◽

Stimulation Of

Chronic obstructive pulmonary disease (COPD) is a chronic respiratory disease with high morbidity and mortality worldwide. So far, smoking is still its leading cause. The characteristics of COPD are emphysema and airway remodeling, as well as chronic inflammation, which were predominated by macrophages. Some studies have reported that macrophages were involved in emphysema and chronic inflammation, but whether there is a link between airway remodeling and macrophages remains unclear. In this study, we found that both acute and chronic cigarette smoke exposure led to an increase of macrophages in the lung and a decrease of ciliated cells in the airway epithelium of a mouse model. The results of in vitro experiments showed that the ciliary protein (β-tubulin-IV) levels of BEAS-2B cells could be inhibited when co-cultured with human macrophage line THP-1, and the inhibitory effect was augmented with the stimulation of cigarette smoke extract (CSE). Based on the results of transcriptome sequencing, we focused on the protein, bone morphogenetic protein-2 (BMP-2), secreted by the macrophage, which might mediate this inhibitory effect. Further studies confirmed that BMP-2 protein inhibited β-tubulin-IV protein levels of BEAS-2B cells under the stimulation of CSE. Coincidentally, this inhibitory effect could be nearly blocked by the BMP receptor inhibitor, LDN, or could be interfered with BMP-2 siRNA. This study suggests that activation and infiltration of macrophages in the lung induced by smoke exposure lead to a high expression of BMP-2, which in turn inhibits the ciliary protein levels of the bronchial epithelial cells, contributing to the remodeling of airway epithelium, and aggravates the development of COPD.

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