Omalizumab may decrease the thickness of the reticular basement membrane and fibronectin deposit in the bronchial mucosa of severe allergic asthmatics

Abstract

Introduction: Immunoglobulin E is an important modulator of the inflammatory reaction in allergic asthma. It also contributes to airway remodeling in the course of the disease. The authors evaluated airway structural changes in severe allergic asthma during the omalizumab therapy. Patients and methods: The study included 13 patients with severe allergic asthma treated with omalizumab for at least one year. In each patient clinical, laboratory, and spirometry parameters were evaluated before and after the treatment. In addition, bronchoscopy with bronchial mucosa biopsy and bronchoalveolar lavage was performed. The basal lamina thickness, inflammatory cell infiltration, fibronectin, as well as type I and III collagen accumulation were assessed in bronchial mucosa specimens, together with the assessment of bronchoalveolar lavage cellularity. Results: The omalizumab therapy led to a decrease in the basal lamina thickness (p = 0.002), and to a reduction in fibronectin (p = 0.02), but not collagen deposits in the bronchial mucosa. The decrease in fibronectin accumulation was associated with an improvement in asthma control and quality of life (p = 0.01, both), and a diminished dose of systemic corticosteroids (p = 0.001). It was also associated with a tendency towards reduction of the eosinophil count in the peripheral blood, bronchoalveolar lavage fluid, and bronchial mucosa specimens. Conclusion: Our study has shown that omalizumab, effective in the treatment of severe allergic asthma, may also decrease unfavorable structural airway changes in allergic asthmatics, at least with respect to the fibronectin deposit and an increased thickness of the basal lamina. However, more extensive observational studies are needed to verify the above hypothesis.

Keywords:

• Asthma
• omalizumab
• airway remodeling
• fibronectin
• IgE

Acknowledgements

We wish to thank various people for their contribution to this project: Anna Andrychiewicz- coordinating nurse in the Bronchoscopy Laboratory, for valuable technical support on this project, and Anna Rams for help in data collection.

Disclosure statement

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

Funding

This project was funded by the National Science Centre based on decision No: DEC-2013/09/B/NZ5/00758 (to S. B-S.).

Authors’ contribution

Weronika Zastrzeżyńska, Krzysztof Sładek, and Jerzy Soja contributed Study Design.

Weronika Zastrzeżyńska, Marek Przybyszowski, Stanisława Bazan-Socha, Agnieszka Gawlewicz-Mroczka, and Jerzy Soja contributed Data Collection.

Weronika Zastrzeżyńska, Stanisława Bazan-Socha, Adam Ćmiel, and Jerzy Soja contributed Statistical Analysis.

Weronika Zastrzeżyńska, Stanisława Bazan-Socha, Krzysztof Sładek, and Jerzy Soja contributed Data Interpretation.

Weronika Zastrzeżyńska, Stanisława Bazan-Socha, Krzysztof Sładek, Jacek Musiał, and Jerzy Soja Manuscript Preparation.

Weronika Zastrzeżyńska, Stanisława Bazan-Socha, and Jerzy Soja contributed Literature Search.

Krzysztof Sładek and Jerzy Soja contributed Bronchofiberoscopy.

Krzysztof Okoń contributed Histology and immunohistochemistry.

Piotr Sadowski and Krzysztof Okoń contributed Cells count.

Bogdan Jakieła and Hanna Plutecka contributed BAL analysis.