Effect of experimental rhinovirus 16 colds on airway hyperresponsiveness to histamine and interleukin‐8 in nasal lavage in asthmatic subjects in vivo

Abstract

We conclude that the severity of cold, as induced by experimental RV16 infection, is a determinant of the increase in airway hypersensitivity to histamine in patients with asthma. Our results suggest that this may be mediated by an inflammatory mechanism, involving the release of chemokines such as IL-8.

Role of nasal nitric oxide in the resolution of experimental rhinovirus infection

“…These findings are consistent with those of previous studies demonstrating that HRV infection in the nose might result in infection in the lower airway as well. [18][19][20][21][22][23][24][25] In the present study symptoms occurred within a day of viral infection, and the time to peak symptoms was 2 to 4 days. There was a highly significant relationship between symptoms and viral load, with both peaking after 2 days.…”

Mode of dendritic cell activation: The decisive hand in Th2/Th17 cell differentiation. Implications in asthma severity?

“…VEGF induces DC maturation and secretion of Th17 promoting cytokines like IL-6 ( Kim et al 2010). Up to 50% of asthma exacerbations are associated with viral infections (Grünberg et al 1997). Binding of viruses has been shown to specifically induce CXCL8 secretion by airway epithelium cells, thereby inducing neutrophil inflammation (Newcomb et al 2005).…”

Effects of viral respiratory infections on lung development and childhood asthma

“…Of particular interest is evidence that activated neutrophils, through the release of the potent secretagogue elastase, can upregulate goblet cell secretion of mucus. 55 Moreover, changes in IL-8 levels in nasal secretions have been related to respiratory symptoms and virus-induced increases in airway hyperresponsiveness, 56,57 suggesting that neutrophils and neutrophil activation products contribute to airway obstruction and symptoms during viral infections and exacerbations of asthma.…”