Serum levels of CC16, SP-A and SP-B reflect tobacco-smoke exposure in asymptomatic subjects

Abstract

Since the 16-kDa bronchiolar Clara cell protein (CC16) and the alveolar surfactant-associated proteins (SP)-A and -B leak into the circulation when parenchymal health is disturbed, the aim of this study was to determine whether their serum levels could serve as early peripheral markers of tobacco smoke-induced epithelial injury.Sixty-nine (51 yrs (32-54) median (25-75th percentile)) nonsmokers and 54 (42 yrs (31-53)) asymptomatic smokers were enrolled in the study.Serum levels of SP-A did not differ between subjects (270 (208-389) versus 259 (168-392) mg?L -1 ), however, CC16 levels decreased (10.6 (8.7-14.6) versus 7.6 (6.0-11.2) mg?L -1 ) and SP-B levels increased (2,529 (2,091-2,943) versus 3,053 (2,613-4,188) mg?L -1 ) in the smokers. When tobacco smoke exposure, serum creatinine (renal index), age and sex were used as independent variables, CC16 was negatively influenced by cumulative smoking and positively influenced by age. SP-A and -B were negatively influenced by creatinine and positively influenced by cumulative smoking. Serum SP-B was inversely correlated with forced expiratory volume in one second/vital capacity, suggesting an association between obstructive disease and parenchymal lung health.The authors suggest that serum surfactant-associated proteins-A and -B reflect increased alveolocapillary leakage whereas Clara cell secretory protein 16 reflects tobacco smoke-induced Clara cell toxicity. Their evaluation may allow the effects of tobacco smoke on different levels of the respiratory tract, cellular toxicity and epithelial leakage to be distinguished.

Study of Role of Surfactant Protein-D, Malondialdehyde, Protein Carbonyl and its Correlation with Airflow Obstruction (FEV1% Predicted) in Patients with Smoker Chronic Obstructive Pulmonary Disease (COPD)

“…In our study we found increase levels of SP-D in patients with smoker COPD and non-smoker COPD this might be due to deleterious effects oxidants from tobacco smoke and oxidants originated from endogenous sources on lung tissue cause release of SP-D in blood stream. The increased level of SP-D in the blood stream depends on the extent of injury to the lung tissue and is directly related to pulmonary function [25][26][27]. In our study we obtain inverse correlation between SP-D with FEV1% predicted and FEV1/FVC % ratio in COPD patients.…”

Diagnostic and prognostic values of Club cell protein 16 (CC16) in critical care patients with acute respiratory distress syndrome

“…Previous studies indicate that circulating CC16 levels are decreased in lung injures caused by agents like tobacco or hexavalent chromium 20, 21. Chronic exposure to toxic agents causes a decline in the overall Clara cells located in terminal and respiratory bronchioles, leading to a relatively low production level of circulating CC16.…”

Urine Club Cell 16-kDa Secretory Protein and Childhood Wheezing Illnesses After Lower Respiratory Tract Infections in Infancy

“…The variables to be included in the multivariable models (age, sex, and current exposure to SHS) were selected a priori based on the published literature. 12,26,37 Due to the relatively small sample size, more variables in the same multivariable models could not be included, but additional analysis replacing current exposure to SHS with other potential confounders (such as maternal asthma or BSS) did not change the results (data not shown). Urine levels of CC16 could be also affected by several other factors (e.g., post-renal excretion of CC16, diurnal variation, and physical activity).…”

“…The variables to be included in the multivariable models (infant's age, sex, and current exposure to SHS) were selected a priori based on published literature. 12,26,29,37 First-order interactions were tested for between urine levels of CC16 and each of the covariates mentioned above.…”

“…13,14 For instance, respiratory disorders that increase the epithelial permeability (e.g., acute respiratory distress syndrome, 16 exposure to proinflammatory agents, 17 or severe chest trauma 18 ) have been associated with higher serum levels of CC16. On the other hand, respiratory illnesses leading to small airway inflammation (e.g., asthma, [19][20][21][22][23][24] exposure to tobacco smoke, [25][26][27] or chronic obstructive pulmonary disease 25,[27][28][29] ) have been associated with lower serum levels of CC16.…”