Dr Nathan Bartlett, Ph.D,
Senior Lecturer,
School of Biomedical Sciences and Pharmacy,
University of Newcastle,
New Lambton Heights, Australia.
Date: Friday, 26 June, 2015
Time: 12:30 pm – 1:30 pm
Venue: MD6-01-02
Chairperson: A/Prof. Fred Wong
Rhinovirus infected epithelium fires up type-2 immunity in asthma
Current therapies prevent only ~40% of asthma exacerbations. The vast majority of asthma exacerbations therefore continue to occur despite use of the best available current therapies. When exacerbations do occur, treatment options are limited and have developed little in recent years. Treatment involves increasing doses of inhaled bronchodilators and systemic/oral corticosteroids – more of the same drugs that failed to prevent the exacerbation occurring in the first place. Virus infections are the major precipitants of exacerbations of asthma: Respiratory virus infections are detected in at least 80% of acute exacerbations in children and adults. Rhinoviruses (RV) are numerically the most important viruses implicated, accounting for 2/3 of infections detected. RV infection is therefore the greatest single precipitant of acute asthma exacerbations. The airway epithelium is the site of RV infection and is now the focus of research seeking to develop better treatments for asthma attacks. We hypothesize that the bronchial epithelium from allergic asthmatics responds fundamentally differently to non-asthmatic epithelium during RV infection. Infection of asthmatic BECs generates an immune mediator milieu involving IL-25 and IL-33 that overcomes control by corticosteroids and activates type-2 immunity leading to increased airways inflammation and worsening of asthma symptoms.
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