Immune Responses in Rhinovirus-Induced Asthma Exacerbations

Abstract

Acute asthma exacerbations are responsible for urgent care visits and hospitalizations; they interfere with school and work productivity, thereby driving much of the morbidity and mortality associated with asthma. Approximately 80 to 85 % of asthma exacerbations in children, adolescents, and less frequently adults are associated with viral upper respiratory tract viral infections, and rhinovirus (RV) accounts for ∼60-70 % of these virus-associated exacerbations. Evidence suggests that it is not the virus itself but the nature of the immune response to RV that drives this untoward response. In particular, evidence supports the concept that RV acts to exacerbate an ongoing allergic inflammatory response to environmental allergens present at the time of the infection. The interaction of the ongoing IgE- and T cell-mediated response to allergen superimposed on the innate and adaptive immune responses to the virus and how this leads to triggering of an asthma exacerbation is discussed.

Keywords: Adaptive immunity; Asthma; Innate immunity; Pathogenesis; Rhinovirus; Viral-induced asthma exacerbations.

Fig. 1

RV-specific T cell proliferation in healthy volunteer. Representative flow cytometry showing IL-4 and IFN-γ expression in T cells (CD4) that were co-cultured with RV-pulsed DCs for 7 days. The x-axis displays cell proliferation as measured by carboxyfluorescein succinimidyl ester (CFSE) dilution with the y-axis demonstrating intracellular cytokine expression. Adapted from [69••].