Low Yield of Pulmonary Surfactant in Cigarette Smokers

Finley, Theodore N.; Ladman, Aaron J.

doi:10.1056/nejm197202032860501

Cited by 130 publications

(74 citation statements)

References 18 publications

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“…Our findings, demonstrating inhibition of stimulated secretion of surfactant following cigarette smoke exposure, correlate with results of whole animal studies, demonstrating unimpaired incorporation of surfactant precursors [5], as well as with clinical reports showing decreased surfactant phospholipids in the lavage fluid of smokers [1][2][3]. This is the first report, however, linking cigarette smoke exposure directly to impaired surfactant secretion from type II cells.…”

Section: Discussionsupporting

confidence: 89%

“…However, the influence of cigarette smoking on the surfactant system has not been well established. Cessation of smoking resulted in a return of the amount of phospholipids to normal levels within 2 weeks [1]. It has been suggested, that structural changes in the lungs of smokers might be responsible for the observed reduction in phospholipid yield [4], but it seems unlikely that these changes would reverse within a short period.…”

mentioning

confidence: 99%

“…Evidence that the yield of surfactant-associated phospholipids in bronchoalveolar lavage fluid of young smokers is reduced compared to healthy controls dates back more than 20 yrs [1], and has recently been confirmed [2,3]. However, the influence of cigarette smoking on the surfactant system has not been well established.…”

mentioning

confidence: 99%

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Acute influence of cigarette smoke on secretion of pulmonary surfactant in rat alveolar type II cells in culture

Wirtz

Schmidt²

1996

Eur Respir J

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It has been shown, that smoking results in a lower yield of surfactant associated phospholipids in bronchoalveolar lavage (BAL). Indirect evidence suggests impaired secretion. In the present study, we investigated the influence of cigarette smoke on surfactant secretion in cultured rat alveolar type II cells.Smoke exposure was achieved by bubbling the smoke of four cigarettes through Dulbecco's modified Eagle's medium (DMEM) which was adjusted to a reference absorption value of 1.36 at 320 nm. Cells were preincubated with various dilutions of cigarette smoke-treated medium for 30 min, and were then exposed to this medium for 2 h. After this time, secretion of 3 H-choline-labelled phosphatidylcholine (PC) was measured as a marker of surfactant secretion.A 10 fold dilution of cigarette smoke-treated medium inhibited PC secretion stimulated by a combination of terbutaline, adenosine triphosphate and 12-O-tetradecanoylphorbol-13-acetate by over 50%, but did not alter basal secretion. Exposure to less concentrated cigarette smoke-treated medium resulted in less inhibition. Cellular injury was not observed with the concentrations of cigarette smoke-treated medium used in this study. The gas phase of cigarette smoke was not inhibitory at comparable concentrations. Longer exposure to cigarette smoke-treated medium resulted in increased inhibition of PC secretion. The cigarette smoke ingredients, nicotine and benzo[a]pyrene, failed to inhibit PC secretion. Secretion of type II cells exposed to cigarette smoke-treated medium at lower temperatures was not affected. Addition of antioxidants to medium and cells during the preincubation and secretion period did not alter cigarette smoke-treated medium-induced inhibition of stimulated PC secretion.These results demonstrate a direct inhibitory effect of cigarette smoke constituents on surfactant secretion in type II cells. Inhibition is mediated by compounds contained predominantly in the particulate phase of cigarette smoke. Inactivation of the inhibitory effect by lower temperatures suggests involvement of processes such as enzymatic bioactivation or active transport mechanisms.

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Section: Discussionsupporting

confidence: 89%

mentioning

confidence: 99%

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Acute influence of cigarette smoke on secretion of pulmonary surfactant in rat alveolar type II cells in culture

Wirtz

Schmidt²

1996

Eur Respir J

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“…As it is known, cigarette smoking is strongly associated with the development of COPD and lung cancer. Smoking can induce alterations of the surfactant system (Finley and Ladman, 1972;Low et al, 1978) and these alterations may be more serious if the composition of the surfactant system is disturbed. The carcinogenic process of lung cancer is driven by the interaction of exogenous carcinogenic exposures and the cellular response, including genetic DNA repair capacity.…”

Section: Discussionmentioning

confidence: 99%

Surfactant protein B gene variations enhance susceptibility to squamous cell carcinoma of the lung in German patients

Seifart

Plagens

et al. 2002

Br J Cancer

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Genetic factors are thought to influence the risk for lung cancer. Since pulmonary surfactant mediates the response to inhaled carcinogenic substances, candidate genes may be among those coding for pulmonary surfactant proteins. In the present matched case -control study a polymorphism within intron 4 of the gene coding for surfactant specific protein B was analysed in 357 individuals. They were divided into 117 patients with lung cancer (40 patients with small cell lung cancer, 77 patients with non small cell lung cancer), matched controls and 123 healthy individuals. Surfactant protein B gene variants were analysed using specific PCR and cloned surfactant protein B sequences as controls. The frequency of the intron 4 variation was similar in both control groups (13.0% and 9.4%), whereas it was increased in the small cell lung cancer group (17.5%) and the non small cell lung cancer group (16.9%). The gene variation was found significantly more frequently in patients with squamous cell carcinoma (25.0%, P=0.016, odds ratio=3.2, 95%CI=1.24 -8.28) than in the controls. These results indicate an association of the surfactant protein B intron 4 variants and/or its flanking loci with mechanisms that may enhance lung cancer susceptibility, especially to squamous cell carcinoma of the lung.

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“…On examining whether these "contaminating" cells might affect the results of the BAM cytotoxicity assay it was found that PMNL were cytotoxic for the A549 target cells but lymphocytes were not. The pathological changes accompanying many of the pulmonary diseases and also smoking habits cause variations in mucus and/or surfactant secretion (Finley & Ladman, 1972;Wanner, 1977). These substances affected attempts to purify BAM by adherence to plastic as removal of non-adherent cells was usually accompanied by loss of most of the BAM which x 0 0 U adhere avidly in aggregates to the mucus or surfactant (Hocking & Golde, 1979b).…”

Section: Discussionmentioning

confidence: 99%

Human bronchoalveolar macrophage cytotoxicity for cultured human lung-tumour cells

Swinburne¹,

Moore²,

Cole³

1982

Br J Cancer

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Human bronchoalveolar macrophages were separated from other free lung cells by density sedimentation on Percoll gradients. They were then tested for cytotoxicity against the human lung adenocarcinoma cell line A549, using a Selenomethionine-75 post-labelling assay. The cytotoxicity of the macrophages increased as the effector:target cell ratio was increased, approaching 100% at 20:1. There was no significant difference in the cytotoxicity of macrophages isolated from the lungs of bronchial-carcinoma or non-carcinoma patients. The highly cytotoxic nature of the macrophages was not due to selection of a more potent cytotoxic subpopulation of macrophages on the Percoll gradient, nor to a generally elevated activation of the macrophages due to the pathological conditions in the patients' lungs. An attempt to determine whether low concentrations of macrophages could potentiate target-cell growth proved negative. Cytotoxicity of macrophages for cultured lung target cells was not restricted to A549 cells and is not in accordance with the view that defective bronchoalveolar macrophage cytotoxicity contributes to the emergence of bronchial neoplasia.

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Low Yield of Pulmonary Surfactant in Cigarette Smokers

Cited by 130 publications

References 18 publications

Acute influence of cigarette smoke on secretion of pulmonary surfactant in rat alveolar type II cells in culture

Acute influence of cigarette smoke on secretion of pulmonary surfactant in rat alveolar type II cells in culture

Surfactant protein B gene variations enhance susceptibility to squamous cell carcinoma of the lung in German patients

Human bronchoalveolar macrophage cytotoxicity for cultured human lung-tumour cells

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