Tobacco Smoke Toxicity: Loss of Human Oral Leukocyte Function and Fluid-Cell Metabolism

Eichel, Bertram; Shahrik, H.A.

doi:10.1126/science.166.3911.1424

Cited by 83 publications

(40 citation statements)

References 12 publications

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“…It is clear from previous studies that the chemotaxis and the phagocytic ability of neutrophils in peripheral blood or saliva are lowered [32,33], while the production of reactive oxygen species is increased in smokers [34,35]. It was also reported that smoking increases PGE 2 , neutrophil elastase [36] and TNF-a levels.…”

Section: Discussionmentioning

confidence: 93%

Matrix remodeling response of human periodontal tissue cells toward fibrosis upon nicotine exposure

et al. 2014

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It is widely accepted that fibrosis is frequently observed in the gingiva of smokers. However, the mechanisms by which smoking results in pathological changes in periodontal tissue that lead to fibrosis are not entirely clear. Our former report showed that type I collagen synthesis was promoted by nicotine via CCN family protein 2 in human periodontal tissue cells. Here, we evaluated other aspects of nicotine function from a viewpoint of extracellular matrix (ECM) remodeling. Human gingival fibroblasts (n = 4) and periodontal ligament cells (n = 3) were isolated. The cells were treated with nicotine at a variety of concentrations for 12-48 h. Modulators of matrix remodeling were measured using enzyme-linked immunosorbent assays. Cell migration and morphology were also evaluated. As a result, following treatment with 1 μg/ml nicotine, tissue inhibitor of metalloproteinase-1 and transforming growth factor-β1 production in both cell lysates and supernatants, and matrix metalloproteinases-1 production in cell lysates, were significantly increased (p < 0.05). Compared to controls, cell migration was significantly inhibited (p < 0.005) by nicotine in a time-dependent manner. Electron microscopic analysis revealed the presence of a number of vacuoles in nicotine-treated cells. These results indicate that nicotine not only impairs fibroblast motility, and induces cellular degenerative changes, but also alters ECM-remodeling systems of periodontal cells. Induction of matrix remodeling molecules, combined with type I collagen accumulation, may account for the molecular mechanism of nicotine-induced periodontal fibrosis.

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Section: Discussionmentioning

confidence: 93%

Matrix remodeling response of human periodontal tissue cells toward fibrosis upon nicotine exposure

et al. 2014

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“…Polymorphonuclear leukocytes from the peripheral blood of smokers exhibit depressed migration and chemotaxis compared with PMNs from nonsmokers (Noble & Penny, 1975;Corberand et al, 1979). The motility and chemotaxis of PMNs are depressed in the oral cavity of smokers compared with nonsmokers (Eichel & Shahrik, 1969;Noble & Penny, 1975). The whole cigarette smoke, its gas phase and the water-soluble fraction are potent inhibitors of PMN chemotaxis (Bridges et al, 1977).…”

Section: Cell-mediated Immune Responsesmentioning

confidence: 99%

Cigarette Smoking and Lower Respiratory Tract Infection

Saldías¹,

Díaz²

2011

Bronchitis

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“…Oceanogr. 3, 448 (1973 smoking include reduced early phase of particle clearance (5), increased closing volume (6), increased airway resistance (7), and toxic effects on oral leukocytes (8). We now report that in hamsters inhaled cigarette smoke recruits polymorphonuclear (PMN) leukocytes to airway lumens from trachea to terminal bronchioles.…”

mentioning

confidence: 99%

Leukocyte Recruitment to Airways by Cigarette Smoke and Particle Phase in Contrast to Cytotoxicity of Vapor

Kilburn

McKenzie

1975

Science

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After hamsters had breathed fresh cigarette smoke in a miniature chamber, airways of the lung showed recruitment of polymorphonuclear leukocytes. Exposure to particles alone by removal of the vapor phase with charcoal did not change the leukocyte response. However, exposure to cigarette smoke vapor after removal of particles with Cambridge filters did not recruit leukocytes but produced nuclear and cytoplasmic vacuoles, double nuclei, and exfoliation of cells.

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Tobacco Smoke Toxicity: Loss of Human Oral Leukocyte Function and Fluid-Cell Metabolism

Cited by 83 publications

References 12 publications

Matrix remodeling response of human periodontal tissue cells toward fibrosis upon nicotine exposure

Matrix remodeling response of human periodontal tissue cells toward fibrosis upon nicotine exposure

Cigarette Smoking and Lower Respiratory Tract Infection

Leukocyte Recruitment to Airways by Cigarette Smoke and Particle Phase in Contrast to Cytotoxicity of Vapor

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