title: Human airway smooth muscle cells express the high affinity receptor for IgE (Fc epsilon RI): a critical role of Fc epsilon RI in human airway smooth muscle cell function.
abstract: Several reports suggest that activated airway smooth muscle (ASM) cells are capable of generating various proinflammatory mediators, including cytokines and chemokines. However, little is known about the mechanism involved in this process. In this regard, we have examined the expression and the role of the high affinity IgE receptor (Fc epsilonRI) by ASM cells. Human ASM cells were found to constitutively express transcripts coding for alpha, beta, and gamma subunits of Fc epsilonRI. Flow cytometry and Western blot analysis confirmed the expression of Fc epsilonRI alpha-chain protein. Interestingly, Fc epsilonRI alpha-chain immunoreactivity was also demonstrated in smooth muscle within bronchial biopsies of asthmatic subjects. Cross-linking of Fc epsilonRI induced mobilization of free calcium in ASM cells, one of the critical signals to trigger smooth muscle contraction. Furthermore, cultured ASM cells released IL-4, IL-13, IL-5, and eotaxin but not IFN-gamma, when sensitized with IgE followed by anti-IgE Ab cross-linking. The addition of anti-Fc epsilonRI alpha-chain Abs directed against IgE binding site inhibited this release. Taken together, these results suggest a potential new and important mechanism by which ASM cells may participate in airway inflammation and bronchoconstriction associated with allergic asthma.
authors.affiliation: Department of Immunology, Section of Respiratory Diseases, Faculty of Medicine, University of Manitoba, Winnipeg Canada.
authors.forename: Abdelilah Soussi
authors.initials: AS
authors.lastname: Gounni
authors.forename: Vincent
authors.initials: V
authors.lastname: Wellemans
authors.forename: Jia
authors.initials: J
authors.lastname: Yang
authors.forename: Fabienne
authors.initials: F
authors.lastname: Bellesort
authors.forename: Kamrouz
authors.initials: K
authors.lastname: Kassiri
authors.forename: Sophie
authors.initials: S
authors.lastname: Gangloff
authors.forename: Moncef
authors.initials: M
authors.lastname: Guenounou
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Halayko
authors.forename: Qutayba
authors.initials: Q
authors.lastname: Hamid
authors.forename: Bouchaib
authors.initials: B
authors.lastname: Lamkhioued
mesh_terms: D001249:Asthma / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D001980:Bronchi / Q000276:immunology* / Q000378:metabolism* / Q000473:pathology; D016535:Bronchial Hyperreactivity / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D020013:Calcium Signaling / Q000276:immunology; D002478:Cells, Cultured; D018925:Chemokines / Q000378:metabolism; D003432:Cross-Linking Reagents / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D006801:Humans; D007073:Immunoglobulin E / Q000378:metabolism; D007424:Intracellular Fluid / Q000276:immunology / Q000378:metabolism; D009119:Muscle Contraction / Q000276:immunology; D009130:Muscle, Smooth / Q000166:cytology / Q000276:immunology* / Q000378:metabolism*; D011485:Protein Binding / Q000276:immunology; D020033:Protein Isoforms / Q000096:biosynthesis; D012333:RNA, Messenger / Q000096:biosynthesis; D017455:Receptors, IgE / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D018418:Th2 Cells / Q000276:immunology / Q000378:metabolism; D014132:Trachea / Q000166:cytology / Q000276:immunology* / Q000378:metabolism*
chemical_list: D018925:Chemokines; D003432:Cross-Linking Reagents; D016207:Cytokines; D020033:Protein Isoforms; D012333:RNA, Messenger; D017455:Receptors, IgE; D007073:Immunoglobulin E