Source: International Congress 2014 – New mechanisms in the pathogenesis of asthma and other lung diseases
Disease area: Airway diseases

Abstract

Background: Smooth muscle cell hypertrophy contributes significantly to airway wall thickness in asthma. It has been postulated that IgE in serum of asthma patients can stimulate airway smooth muscle cell proliferation even when no antigens are present. In this study we tested if the therapeutically used humanized anti-IgE antibody Omalizumab can reduce smooth muscle cell growth induced by asthmatic serum.Methods: Using isolated primary human airway smooth muscle cells obtained from asthma patients (n=7) and non-asthmatic controls (n=7) we stimulated proliferation with either: i) 5% fetal calf serum (FCS), ii) pooled human serum (PHS), or iii) serum obtained from asthma patients (APS) over 3 and 5 days. Cell numbers were determined by manual cell counts using an improved Neugbaur chamber slide.Results: Compared to FCS human sera were significant stronger inducers of cell proliferation (p<0.05), with APS being stronger than PHS (p<0.001) Furthermore, APS induced a significant faster proliferation of smooth muscle cells when the cells were obtained from asthma patients compared to non-asthma controls (p<0.01). Pre-incubation of APS with Omalizumab dose-dependently reduced the pro-proliferative effect in cells of both asthma patients and of non-asthma controls. The effect was also dependent on the length of pre-incubation of APS with Omalizumab. No reducing effect of Omalizumab was observed in cells stimulated with either FCS or PHS, suggesting that the proliferative effect of APS was directly dependent on the content of IgE.Conclusion: Our data indicates that Omalizumab has the potential to reduce asthma related smooth muscle cell hypertrophy and thus reduce airway wall thickening in long term therapy.

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Citations should be made in the following way:
M. Roth, J. Zhong, M. Tamm (Basel, Switzerland). Omalizumab prevents smooth muscle cell growth induced by asthmatic serum. Eur Respir J 2014; 44: Suppl. 58, 3871

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