Rhinovirus and Asthma

Abstract

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.

Cardiac ICAM-1 mediates leukocyte-dependent decreased ventricular contractility in endotoxemic mice☆

“…Maximum production of ICAM-1 occurs 18 to 24 h after cytokine stimulation [8]. Ligands for ICAM-1 include CD11/CD18 receptors [26,29,30], fibrinogen [31], rhinovirus receptors [32] and plasmodium falciparum [33].…”

The role of rhinovirus in asthma exacerbations

“…20,21 Papadopoulos et al 10 found local induction of proinflammatory mediators that could provide a mechanism to explain how lower airway infection can lead to inflammation and asthma. RV infection resulted in an increase in mRNA expression and subsequent translation of IL-6, IL-8, and IL-16.…”

Erythromycin ameliorates renal injury via anti-inflammatory effects in experimental diabetic rats

“…Low-dose and long-term therapy with erythromycin, which reduces ICAM-1 expression in the airway epithelial cells and inhibits rhinovirus infection, is effective for chronic obstructive pulmonary disease, diffuse panbronchiolitis and chronic sinusitis [14][15][16][17]. It has also been reported that macrolides reduce the progression of bleomycin-induced lung injury in mice by inhibiting the induction of adhesion molecules, and neutrophil and macrophage migration into the airspace [18,19].…”