Cigarette smoke affects dendritic cell maturation in the small airways of patients with chronic obstructive pulmonary disease

Abstract

The aim of the present study was to characterize and quantify the numbers and expression levels of cells markers associated with dendritic cell (DC) maturation in small airways in current smokers and non-smokers with or without chronic obstructive pulmonary disease (COPD). Lung tissues from the following 32 patients were obtained during resection for lung cancer: Eight smokers with COPD, eight non-smokers with COPD, eight current smokers without COPD and eight non-smokers without COPD, serving as a control. The tissue sections were immunostained for cluster of differentiation (CD)83+ and CD1a+ to delineate mature and immature DCs, and chemokine receptor type 7 (CCR7+) to detect DC migratory ability. Myeloid DCs were collected from the lung tissues, and subsequently the CD83+ and CCR7+ expression levels in the lung myeloid DCs were detected using flow cytometry. The expression levels of CD83+, CD1a+ and CCR7+ mRNA in total lung RNA were evaluated by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Evident chronic bronchitis and emphysema pathological changes were observed in the lung tissues of patients with COPD. The results revealed that the numbers of CD83+ and CCR7+ DCs were reduced but the numbers of CD1a+ DCs were significantly increased in the COPD group as compared with the control group (P<0.05, respectively). Using RT-qPCR, the expression levels of CCR7+ and CD83+ mRNA were found to be reduced in the smokers with COPD as compared with the non-smokers without COPD group (P<0.05, respectively). Excessive local adaptive immune responses are key elements in the pathogenesis of COPD. Cigarette smoke may stimulate immune responses by impairing the homing of airway DCs to the lymph nodes and reduce the migratory potential of DCs. The present study revealed that COPD is associated with reduced numbers of mature CD83+ DCs and lower CCR7+ expression levels in small airways.

An assessment of the relationship between the expression of CCR7/CCL19 axis and selected regulatory miRNAs in non-small cell lung cancer

“…This is the first study to examine CCR7 mRNA expression in NSCLC patients in relation to smoking history, which revealed higher expression level in patients with a smoking status ≥ 40PYs (see Table 3). Previous studies focused on exposure of patient with chronic obstructive pulmonary disease to cigarette smoke have suggested that cigarette smoke may have an influence on CCR7 expression [15].…”

Expression of the Lymphocyte Chemokine XCL1 in Lung Tissue of COPD Mice, and Its Relationship to CD4+/CD8+ Ratio and IL-2

“…Similar approaches were undertaken by other authors [19,20] who demonstrated pathological changes instead of testing pulmonary function to demonstrate the validity of COPD model. In COPD, main pathological changes are in the small airways, and chronic inflammation is part of these changes [21]. COPD pathophysiology is closely related to infiltration of T lymphocytes in the airways and lung parenchyma [2].…”

Impact of tobacco smoke on upper airway dendritic cell accumulation and regulation by sinonasal epithelial cells

“…Moreover, after smoking cessation, total DC levels were comparable to those of nonsmokers . Likewise, Liao et al demonstrated that, in the small airway, there was a modest decrease in the presence of CD83 + DCs in active smokers with compared with nonsmokers . Given our work demonstrating that smoke had opposing effects on each of the myeloid DC subsets, total myeloid DC counts may not give an accurate representation of tissue populations.…”