Assessment of the Molecular Basis of the Proallergenic Effects of Cigarette Smoke

• Published in: Environmental science & technology Vol. 34; no. 7; pp. 1370 - 1374
• Main Authors: Smyth, Lucy J. C, Machado, Denise C, Upton, Anthony P, Good, Samantha, Aufderheide, Michaela, Helm, Birgit A
• Format: Journal Article
• Language: English
• Published: Washington, DC American Chemical Society 01-04-2000
• Subjects: Allergic diseases; Allergies; Biological and medical sciences; Cells; Cigarettes; Immunopathology; interleukin 13; Medical sciences; Oncogenic viruses; Pollutants; Pulmonary diseases; Respiratory and ent allergic diseases; Smoke inhalation; Tobacco smoke; Tobacco, tobacco smoking; Toxicology; Immunopathology; Allergy; Respiratory disease; Toxicity; IgE; Cytokine; Tobacco smoking; In vitro; Asthma; Tobacco; Mast cell; Obstructive pulmonary disease; Mechanism of action; Fumes
• ISSN: 0013-936X; 1520-5851
• DOI: 10.1021/es9909576

Epidemiological studies indicate a link between smoking and increased risk of immunoglobulin E-mediated allergies and asthma. The molecular basis underlying cigarette smoke related respiratory disorders are ill defined, but it is known that mast cells in the mucosal lining of the airways are an important reservoir of proinflammatory mediators, which play a pivotal role in the development of these diseases. The establishment of a novel cell exposure unit facilitated a study of mast cell responses to pollutants in mainstream cigarette smoke at the air/cell interface. Our study shows that cigarette smoke, but not filtered clean air, induces the release of mediators of type I hypersensitivity responses and stimulates the synthesis of proinflammatory cytokines, including interleukin (IL)-4, 5, 10, and 13 and tumor necrosis factor (TNF)-α, in cells of mast cell lineage. These results explain how exposure to pollutants present in cigarette smoke can induce the pathophysiological responses associated with allergy, IgE-mediated and IgE-independent asthma since IL-4 and IL-13 induce class switching to IgE, and IL-13 has recently been identified as the key mediator of IgE-independent asthma.