Rhinovirus infections: induction and modulation of airways inflammation inasthma

There is renewed interest in the role of respiratory virus infections in th e pathogenesis of asthma and in the development of exacerbations in pre-exi sting disease. This is due to the availability of new molecular and experim ental tools. Circumstantial evidence points towards a potentially causative role as well as to possibly protective effects of certain respiratory viru ses in the cause of allergic asthma during early childhood. In addition, it now has become clear that exacerbations of asthma, in children as well as adults, are mostly associated with respiratory virus infections, with a pre dominant role of the common cold virus: rhinovirus. Careful human in vitro and in vivo experiments have shown that rhinovirus can potentially stimulat e bronchial epithelial cells to produce pro-inflammatory chemokines and cyt okines, may activate cholinergic- or noncholinergic nerves, increase epithe lial-derived nitric oxide synthesis, upregulate local ICAM-1 expression, an d can lead to nonspecific T-cell responses and/or virus-specific T-cell pro liferation. Experimental rhinovirus infections in patients with asthma demo nstrate features of exacerbation, such as lower airway symptoms, variable a irways obstruction, and bronchial hyperresponsiveness, the latter being ass ociated with eosinophil counts and eosinophilic cationic protein levels in induced sputum. This suggests that multiple cellular pathways can be involv ed in rhinovirus-induced asthma exacerbations. It is still unknown whether these mechanisms are a distinguishing characteristic of asthma. Because of the limited effects of inhaled steroids during asthma exacerbations, new th erapeutic interventions need to be developed based on the increasing pathop hysiological knowledge about the role of viruses in asthma.