Serum IgE Induced Airway Smooth Muscle Cell Remodeling Is Independent of Allergens and Is Prevented by Omalizumab |
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Authors: | Michael Roth Feng Zhao Jun Zhong Didier Lardinois Michael Tamm |
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Affiliation: | 1. Pulmonary Cell Research, Department Biomedicine, University Basel, Basel, Switzerland.; 2. Department Internal Medicine, Pneumology, University Hospital Basel, Basel, Switzerland.; 3. Department of Respiratory Diseases, Xijing Hospital, 4th Military Medical University, Xi’an, People’s Republic of China.; 4. Department Thoracic Surgery, University Hospital Basel, Basel, Switzerland.; French National Centre for Scientific Research, FRANCE, |
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Abstract: | BackgroundAirway wall remodeling in allergic asthma is reduced after treatment with humanized anti-IgE-antibodies. We reported earlier that purified IgE, without the presence of allergens, is sufficient to induce airway wall remodeling due to airway smooth muscle cell (ASMC) activity deposing extracellular matrix.ObjectiveWe postulate that IgE contained in serum of allergic asthma patients, in the absence of allergens, stimulates ASMC remodeling activities and can be prevented by anti-IgE antibodies.MethodsIsolated human ASMC were exposed to serum obtained from: (i) healthy controls, or patients with (ii) allergic asthma, (iii) non-allergic asthma, and (iv) atopic non-asthma patients. Proliferation and the deposition of collagens and fibronectin were determined after 3 and 5 days.ResultsSerum from patients with allergies significantly stimulated: (i) ASMC proliferation, (ii) deposition of collagen type-I (48 hours) and (iii) of fibronectin (24 hours). One hour pre-incubation with Omalizumab prevented these three effects of allergic serum, but had no significant effect on serum from healthy donors or non-allergic asthma patients. Interestingly, the addition of allergens did not further increase any of the IgE effects.Conclusion and Clinical RelevanceOur data provides experimental evidence that the beneficial effect of Omalizumab on airway wall remodeling and improved lung function may be due to its direct action on IgE bound ASMC. |
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