Eosinophils Induce Airway Smooth Muscle Cell Proliferation View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2013-04

AUTHORS

Rabih Halwani, Alejandro Vazquez-Tello, Yuki Sumi, Mary Angeline Pureza, Ahmed Bahammam, Hamdan Al-Jahdali, Abdelillah Soussi-Gounni, Bassam Mahboub, Saleh Al-Muhsen, Qutayba Hamid

ABSTRACT

Asthma is characterized by eosinophilic airway inflammation and remodeling of the airway wall. Features of airway remodeling include increased airway smooth muscle (ASM) mass. However, little is known about the interaction between inflammatory eosinophils and ASM cells. In this study, we investigated the effect of eosinophils on ASM cell proliferation. Eosinophils were isolated from peripheral blood of mild asthmatics and non-asthmatic subjects and co-cultured with human primary ASM cells. ASM proliferation was estimated using Ki-67 expression assay. The expression of extracellular matrix (ECM) mRNA in ASM cells was measured using quantitative real-time PCR. The role of eosinophil derived Cysteinyl Leukotrienes (CysLTs) in enhancing ASM proliferation was estimated by measuring the release of leukotrienes from eosinophils upon their direct contact with ASM cells using ELISA. This role was confirmed either by blocking eosinophil-ASM contact or co-culturing them in the presence of leukotrienes antagonist. ASM cells co-cultured with eosinophils, isolated from asthmatics, but not non-asthmatics, had a significantly higher rate of proliferation compared to controls. This increase in ASM proliferation was independent of their release of ECM proteins but dependent upon eosinophils release of CysLTs. Eosinophil-ASM cell to cell contact was required for CysLTs release. Preventing eosinophil contact with ASM cells using anti-adhesion molecules antibodies, or blocking the activity of eosinophil derived CysLTs using montelukast inhibited ASM proliferation. Our results indicated that eosinophils contribute to airway remodeling during asthma by enhancing ASM cell proliferation and hence increasing ASM mass. Direct contact of eosinophils with ASM cells triggers their release of CysLTs which enhance ASM proliferation. Eosinophils, and their binding to ASM cells, constitute a potential therapeutic target to interfere with the series of biological events leading to airway remodeling and Asthma. More... »

PAGES

595-604

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s10875-012-9836-3

DOI

http://dx.doi.org/10.1007/s10875-012-9836-3

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1043094206

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/23180361


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