Authors:
Holt, P. G.; Strickland, D. H.; Sly, P. D.
Authors notes:
Current Opinion in Allergy and Clinical Immunology, 12(2), 151-157.
Keywords:
atopic asthma, IgE receptor, IL-15, virus infection
Abstract
Information is accumulating which implicates airway inflammation resulting from respiratory viral infections, acting against a background of atopy, in both the cause and pathogenesis of atopic asthma.
This review brings together the most recent publications relevant to this rapidly evolving area, particularly those focusing on underlying pathogenic mechanisms.
Salient findings from the recent literature include increased respiratory infection-associated symptom severity/duration and loss of asthma control in atopic relative to nonatopic children; up-regulation of FcεR1 expression on circulating monocytes/dendritic cells occurs during virus-associated atopic asthma exacerbations, providing a mechanism for transient amplification of underlying allergic airways inflammation; high potency of hRV-type C in induction of infection-associated wheeze; Th2-polarized immunity to mucosal dwelling bacteria and protection against asthma; a role for IL-15 in viral-associated airways inflammation; vitamin D and protection against infection-associated asthma exacerbations; strategies for reduction of infection-associated wheezing severity by boosting mucosal Treg cell activity via immunostimulation of the gut mucosa.
Research in this area is pointing towards new rationales for development of early intervention strategies for prevention of asthma initiation and progression in childhood, based on control of respiratory infections and/or sensitization to aeroallergens.