Mechanisms of rhinovirus-induced asthma

摘要: Several epidemiological studies using sensitive detection methodologies have confirmed that the majority of acute asthma exacerbations follow upper respiratory tract infections--common colds. Most these colds are due to human rhinoviruses (RVs). RVs able reach and replicate in epithelial cells lower airways can activate produce pro-inflammatory mediators. Under some circumstances, also become cytotoxic epithelium. Atopic asthmatic individuals less interferon-gamma more interleukin-10 than normal subjects response RV infection. Symptom severity as well viral shedding after experimental infection, is inversely correlated with 'atopic' status, expressed interleukin-5 ratio. Expression co-stimulatory molecules on immune affected atopic asthmatics, suggesting an aberrant may lead suboptimal clearance persistence. Some above effects be reversed vitro by corticosteroids, second-generation antihistamines or anti-oxidants; however, optimal strategy for treating requires further research at both mechanistic clinical levels.