Abstract
Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation and systemic inflammation. The main causes of COPD include interaction between genetic and environmental factors associated with tobacco smoking (COPD-TS) and/or exposure to biomass smoke (COPD-BS). Several microRNAs (miRNAs) control posttranscriptional regulation of COPD-TS associated gene expression. The miR-22-HDAC4-IL-17 axis was recently characterized. It is still unknown, however, whether this axis, participates in COPD-BS. To investigate, 50 patients diagnosed with severe-to-very severe COPD GOLD (Global Initiative for Chronic Obstructive Lung Disease) stages III/IV, were recruited, 25 women had COPD-BS (never smokers, exposed heavily to BS) and 25 had COPD-TS. Serum levels of miRNA-22-3p were measured by RT (Reverse Transcription)-qPCR, while the concentration of HDAC4 (Histone deacetylase 4) was detected by ELISA. Additionally, we looked for association between serum HDAC4 and DLCOsb (Single-breath diffusing capacity of the lung for carbon monoxide), as % of predicted by age, height, and gender, one of the main differences described between COPD-BS and COPD-TS. Women with COPD-BS were older and shorter and had a higher DLCOsb %P (percent predicted) compared to COPD-TS. Serum miR-22-3p was downregulated in COPD-BS relative to COPD-TS. In contrast, the concentration of HDAC4 was higher in COPD-BS compared to COPD-TS. Furthermore, a positive correlation between serum HDAC4 levels and DLCOsb %P was observed. We concluded that the miR-22-HDAC4-DLCO axis behaves differently in patients with COPD-BS and COPD-TS.
Highlights
The main risk factor for the development of chronic obstructive pulmonary disease (COPD) is exposure to tobacco smoke (COPD-TS)
The pathogenesis of COPD begins when the particles of tobacco or biomass smoke are inhaled and deposited deep in the airways and lungs, triggering an inflammatory response, which is perpetuated, evolving towards chronic and irreversible damage that could lead to bronchiolitis and emphysema [3]
Patients with COPD-TS were active smokers or had quit smoking for less than 1 year prior to be enrolled in the study, and were not exposed to biomass smoke
Summary
The main risk factor for the development of chronic obstructive pulmonary disease (COPD) is exposure to tobacco smoke (COPD-TS). The pathogenesis of COPD begins when the particles of tobacco or biomass smoke are inhaled and deposited deep in the airways and lungs, triggering an inflammatory response, which is perpetuated, evolving towards chronic and irreversible damage that could lead to bronchiolitis and emphysema [3]. Women exposed to BS presented more local scarring and pigment deposition in the lung parenchyma, and more fibrosis. These differences have suggested the existence of two clearly distinct phenotypes of COPD, one linked to tobacco smoke and another to biomass [7]
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