Smyth, L.J.L.J.SmythMachado, D.C.D.C.MachadoUpton, A.P.A.P.UptonGood, S.S.GoodAufderheide, M.M.AufderheideHelm, B.A.B.A.Helm2022-03-032022-03-032000https://publica.fraunhofer.de/handle/publica/19828210.1021/es9909576 S0013-936X(99)00957-8Epidemiological studies indicate a link between smoking and increased risk of IgE-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. This 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)-alpha, 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.enair pollutionallergyAsthmacytokinecytotoxicityimmunoglobulinsinterleukinsmast celltobacco smoke615610620628journal article