Ciliary Abnormalities in Bronchial Epithelium of Smokers, Ex-smokers, and Nonsmokers

Abstract

Although respiratory changes induced by tobacco smoke have been extensively described, no study has focused on ciliary abnormalities associated with chronic smoking. Ciliary ultrastructure was studied in 37 adults with chronic sputum production (CSP) consisting of 13 current smokers (Group 1), 5 ex-smokers (Group 2), and 19 nonsmokers (Group 3). Five healthy nonsmokers constituted the control group (Group 4). Clinical and radiologic data and respiratory function tests were recorded. Acute respiratory infection was diagnosed by culture of tracheobronchial secretions obtained during bronchoscopy. Bronchial ciliated cells were obtained and processed for transmission electron microscopy. Within each group, the percentages of abnormal cilia were similar in patients with either chronic bronchitis or bronchiectasis and in patients with or without acute infection. The percentage of axonemal ultrastructural abnormalities (AUA) was higher in smokers (16.5% +/- 2.7%) and ex-smokers (17.5% +/- 7%) than in nonsmokers (5.2% +/- 1%) or control subjects (0.7% +/- 0.2%) (p < 0.0002). The AUA were polymorphic, characteristic of acquired ultrastructural changes. These results suggest that chronic smoking may induce an increased number of abnormal cilia which could participate in impairment of tracheobronchial clearance and which appears to be independent of the etiology of CSP.

The Effects of Smoking Cessation on the Risk of Chronic Obstructive Pulmonary Disease Exacerbations

“…This unadjusted observation fits with previous studies and may be consistent with the hypothesis of improved ciliary function leading to increased sputum production, clearance and symptoms. [28][29][30][31] However, there is also the possibility of an indication bias leading to this finding in that individuals who have smoked for long periods of time often have some factors predisposing to future exacerbations, such as increasing dyspnea or prior exacerbations. Previous COPD exacerbation is a strong predictor of future exacerbations and may account for some of the unadjusted findings.…”

Chronic inflammation in the respiratory tract and ciliary dyskinesia

“…The prolonged exposure to the irritant, e.g. cigarette smoke, while DOI: 10.5114/ceji.2013.34369 affecting epithelial stem cells, may further result in neoplastic transformation of epithelium [10,11].…”

“…Furthermore, numerous other external factors may influence the cilia motility and ciliogenesis in both, direct and indirect manner. Among a broad range of air pollution constituents, an important position have toxic components of tobacco smoke [27,41,42]. In addition to well documented negative direct influence on a structure and motility of cilia it was proven that tobacco smoke components decrease the cilia number [43,44], and affect their regeneration [45].…”

Mechanisms of the innate immunity in the respiratory system

“…Based on the origin of mentioned abnormalities, the inherited, genetically determined changes are classified as primary ciliary diskinesia (PCD), whereas the acquired, usually associated with various detrimental factors (e.g. infection, allergy, or chronic exposure to tobacco smoke) are characterized as secondary ciliary dyskinesia (SCD) [37][38][39][40][41].…”