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Absorption of Nasal and Bronchial Fluids: Precision Sampling of the Human Respiratory Mucosa and Laboratory Processing of Samples
Published on: January 21, 2018
Asthmatic bronchial smooth muscle increases rhinovirus replication within the bronchial epithelium
Pauline Esteves1, Benoit Allard1, Alexis Celle1
1Univ-Bordeaux, Centre de Recherche Cardio-thoracique de Bordeaux, U1045, Département de Pharmacologie, CIC 1401, 33000 Bordeaux, France; INSERM, Centre de Recherche Cardio-thoracique de Bordeaux U1045, Plateforme Transcriptome Neurocentre Magendie U1215, Functionnal Genomics Center (CGFB) Proteomics Facility, CIC 1401, PTIB - Hôpital Xavier Arnozan, Avenue du Haut Lévêque, 33600 PESSAC, 33000 Bordeaux, France.
Abstract:
Rhinovirus (RV) infection of the bronchial epithelium is implicated in the vast majority of severe asthma exacerbations. Interestingly, the susceptibility of bronchial epithelium to RV infection is increased in persons with asthma. Bronchial smooth muscle (BSM) remodeling is an important feature of severe asthma pathophysiology, and its reduction using bronchial thermoplasty has been associated with a significant decrease in the exacerbation rate. We hypothesized that asthmatic BSM can play a role in RV infection of the bronchial epithelium. Using an original co-culture model between bronchial epithelium and BSM cells, we show that asthmatic BSM cells increase RV replication in bronchial epithelium following RV infection. These findings are related to the increased production of CCL20 by asthmatic BSM cells. Moreover, we demonstrate an original downregulation of the activity of the epithelial protein kinase RNA-activated (PKR) antiviral pathway. Finally, we identify a direct bottom-up effect of asthmatic BSM cells on bronchial epithelium susceptibility to RV infection.
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