In Vitro Acute Effects of Tobacco Smoke on Tumor Necrosis Factor a and Interleukin-6 Production by Alveolar Macrophages

Dubar, V.; Gosset, Philippe; Aerts, C; Voisin, C; Wallaert, B.; Tonnel, A. B.

doi:10.3109/01902149309064351

Cited by 58 publications

(41 citation statements)

References 23 publications

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“…Cigarette smokers exhibit reduced SP-D levels (43), elevated MMP levels (44), and reduced alveolar macrophage CD14 levels (45). In addition, human alveolar macrophages in culture produced significantly less TNF-␣ and IL-6 after cigarette smoke exposure (46). This suggests MMP-12 may mediate reduction of alveolar macrophage CD14 and reduced macrophage cytokine production in smokers and other pulmonary diseases characterized by elevated MMPs.…”

Section: Macrophages From Cd14mentioning

confidence: 87%

Surfactant Protein-D Regulates Soluble CD14 through Matrix Metalloproteinase-12

Senft¹,

Korfhagen²,

Whitsett³

et al. 2005

The Journal of Immunology

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Surfactant protein D (SP-D) and CD14 are important innate immune defense molecules that mediate clearance of pathogens and apoptotic cells from the lung. To test whether CD14 expression and function were influenced by SP-D, the surface expression of CD14 was assessed on alveolar macrophages from SP-D−/− mice. CD14 was reduced on alveolar macrophages from SP-D−/− mice and was associated with reduced uptake of LPS and decreased production of TNF-α after LPS stimulation. CD14 is proteolytically cleaved from the cell surface to form a soluble peptide. Soluble CD14 (sCD14) was increased in the bronchoalveolar lavage fluid from SP-D−/− mice. Because matrix metalloproteinase (MMP)-9 and -12 activities were increased in the lungs of SP-D−/− mice, the role of these metalloproteases in the production of sCD14 was assessed. sCD14 was decreased in both MMP9−/−/SP-D−/− and MMP12−/−/SP-D−/− mice demonstrating MMP-9 and MMP-12 contribute to proteolytic shedding of CD14. The increased sCD14 seen in SP-D−/− mice was dependent upon the activation of MMP-12 via an MMP-9-dependent mechanism. Supporting this observation, MMP-12 caused the release of sCD14 from RAW 264.7 cells in vitro. In conclusion, SP-D influences innate host defense, in part, by regulating sCD14 in a process mediated by MMP-9 and MMP-12.

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Section: Macrophages From Cd14mentioning

confidence: 87%

Surfactant Protein-D Regulates Soluble CD14 through Matrix Metalloproteinase-12

Senft¹,

Korfhagen²,

Whitsett³

et al. 2005

The Journal of Immunology

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“…A similar in vitro model was used to study cell injury, protein synthesis and cytokine production in alveolar macrophages [19]. In this study, the 1:15 diluted gas phase smoke of two cigarettes was blown over the cells cultured on a porous support.…”

Section: Discussionmentioning

confidence: 99%

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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“…Thus, the initiation of cytokine release in COPD is likely to be due to the direct effect of cigarette smoking, although, in general, the release of cytokines in COPD patients is higher than that in asymptomatic smokers. Cigarette smoke increases IL-8 gene expression and release by bronchial epithelial cells, and TNF-a and IL-6 by alveolar macrophages [28,29], and oxidants that are present in cigarette smoke cause the release of proinflammatory cytokines such as IL-1 and IL-8 from macrophages and epithelial cells. Exposure of lung epithelial cells to smoke extract causes the release of neutrophilic and monocytic chemotactic activities, with IL-8 and G-CSF accounting for the neutrophilic activity and MCP-1 for the monocytic activity [30].…”

Section: Cytokine Profile In Chronic Obstructive Pulmonary Diseasementioning

confidence: 99%