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The Journal of Immunology, 2005, 175: 2613-2621.
Copyright © 2005 by The American Association of Immunologists

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

Abdelilah Soussi Gounni*, Vincent Wellemans{dagger}, Jia Yang*, Fabienne Bellesort{dagger}, Kamrouz Kassiri*, Sophie Gangloff{ddagger}, Moncef Guenounou{ddagger}, Andrew J. Halayko*, Qutayba Hamid§ and Bouchaib Lamkhioued2,{ddagger}

* Department of Immunology, Department of Physiology, Section of Respiratory Diseases, Faculty of Medicine, University of Manitoba, Winnipeg Canada; {dagger} Ste-Justine Hospital, Research Centre, University of Montreal, Montreal, Quebec Canada; {ddagger} Laboratoire d’Immunologie et Microbiologie, Faculté de Pharmacie, IFR53 Biomolécules, Reims, France; and § Meakins-Christie Laboratories and Departments of Medicine and Pathology, McGill University, Montreal, Quebec Canada.

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{epsilon}RI) by ASM cells. Human ASM cells were found to constitutively express transcripts coding for {alpha}, {beta}, and {gamma} subunits of Fc{epsilon}RI. Flow cytometry and Western blot analysis confirmed the expression of Fc{epsilon}RI {alpha}-chain protein. Interestingly, Fc{epsilon}RI {alpha}-chain immunoreactivity was also demonstrated in smooth muscle within bronchial biopsies of asthmatic subjects. Cross-linking of Fc{epsilon}RI 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{epsilon}RI {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.




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Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
A. S. Gounni
The high-affinity IgE receptor (Fc{epsilon}RI): a critical regulator of airway smooth muscle cells?
Am J Physiol Lung Cell Mol Physiol, September 1, 2006; 291(3): L312 - L321.
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