Rhinoviruses (RVs) cause the majority of common colds, which often provoke wheezing in patients with asthma. The precise mechanisms responsible for the RV infection-induced exacerbations of bronchial asthma are still uncertain. However, several reports reveal airway hyperresponsiveness, increases in chemical mediators in airway secretions such as kinin and histamine, and airway inflammation in patients with bronchial asthma after RV infection. RV infection induces an accumulation of inflammatory cells in airway mucosa and submucosa including neutrophils, lymphocytes and eosinophils. RV affects the barrier function of airway epithelial cells, and activates the airway epithelial cells and other cells in the lung to produce pro-inflammatory cytokines, including various kinds of interleukins, GM-CSF and RANTES, and histamine. RV also stimulates the expression of intercellular adhesion molecule-1 (ICAM-1) and low-density lipoprotein receptors in the airway epithelium, receptors for major and minor RVs. On the other hand, RV infection is inhibited by treatment with soluble ICAM-1, and by reduction of ICAM-1 expression in the airway epithelial cells after treatment with erythromycin. Both soluble ICAM-1 and erythromycin were reported to reduce the frequency of common colds. Here, we review the pathogenesis and management of RV infection-induced exacerbation of bronchial asthma.