RV respiratory infection is an etiologic agent in severe asthma exacerbations necessitating hospitalization in adults. Compared with hospitalized patients with asthma who were RV negative, RV-positive patients were significantly more likely to be smokers and nonusers of ICSs.
Interaction of allergen with T-cells is associated with patterns of cytokine release by immunocompetent cells characterized as T-helper Th1 or Th2 T-immune responses. The Th2 pattern of inflammation induced by this cytokine release is associated with allergic diseases. The molecular mechanisms underlying allergic inflammation are the signals for immunoglobulin (Ig) E production and the activation of mast cells and eosinophils. Data suggesting that environmental exposure may play a role in the induction of the Th2 pattern of inflammation has led to the development of the "hygiene hypothesis." Knowledge of the mechanisms of allergic inflammation has allowed the development of specific pharmacologic intervention to include 1) antibodies to IgE, 2) therapy tailored to regulate IgE production, and 3) modulation of cytokine release and function. Knowledge of the role of transcription factors in regulating gene activity as it relates to allergic inflammation is expanding and may also provide future targets for pharmacologic intervention.
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