Table 2—

Current hypotheses for the pathogenesis of virus-induced asthma exacerbations

Reduced ciliary clearance
Epithelial disruptionIncreased permeability
Loss of protective functions
Kinins
Mediator productionComplement
Arachidonic acid metabolites
Nitric oxide
Reactive oxygen products
Cytokines
Induction of inflammationChemokines
Immune cell activation
Adhesion molecule induction
Increased total IgE
IgE dysregulationAntiviral IgE production
Airway smooth muscle
Airway remodellingFibroblasts
Myofibroblasts
Growth factors
Increased cholinergic sensitivity
Alterations of neural responsesNeuropeptide metabolism modulation
β-Adrenergic receptor dysfunction
  • IgE: immunoglobulin-E