Rhinovirus-Induced Exacerbations of Asthma and COPD

Hershenson, Marc B.

However, the notion that viral infection simply augments asthmatic airway inflammation may not explain why asthmatics suffer manifestations of lower airways disease after colds while normal individuals do not. Could asthmatics Tissue was stained for RV16 capsid protein (red) and DAPI, a nuclear stain. Note that some cells are stained with RV and others are not. (c) Tissue was stained with mouse IgG, a negative control, and DAPI. Note the absence of red staining. Antibody against RV16 and tissue blocks were generously provided by Wai-Ming Lee, Nizar Jarjour, and Jim Gern (University of Wisconsin Figure 2 : A mechanism to explain defective innate immunity in asthma. The differentiation of Th1 and Th2 T-helper cell lineages is mutually antagonistic. Th2 cells produce IL-4 which blocks Th1 differentiation and Th1 cells produce IFN-which blocks Th2 differentiation. Thus, individuals with an immune system skewed towards Th2 tend not to produce eosinophils and IgE-producing B cells, but not Th1 cells. The relative lack of IFN-limits the antiviral response.