Viral infections are the most frequent cause of attacks in asthma – a chronic lung disease characterized by increased inflammation, airway reactivity and mucus production.
To understand how viral infections cause asthma attacks, Vanderbilt investigators previously developed a mouse model of respiratory syncytial virus (RSV) infection during ongoing allergic asthma induced by ovalbumin (OVA). They found that OVA/RSV mice had increased lung expression of the immune factor IL-17A, which is associated with severe asthma and is a therapeutic target of inhibitors currently in clinical trials.
Dawn Newcomb, Ph.D., research assistant professor of Medicine, and colleagues have now investigated the role of IL-17A in airway reactivity and inflammation in the OVA/RSV model. They were surprised to find that in mice missing IL-17A, OVA/RSV increased airway reactivity and the influx of inflammatory cells, compared to the same treatment in wild-type mice.
The findings, reported in the journal Thorax, suggest that IL-17A reduces airway reactivity and inflammation in OVA/RSV mice and that inhibiting IL-17A in the setting of virally-induced asthma attacks may have adverse consequences.
This research was supported by grants from the National Institutes of Health (HL090664, AI070672, AI059108, GM015431, HL106446, AI095227, HD043483) and from the Department of Veterans Affairs.
