作者: K. GRÜnberg , P. J. Sterk
DOI: 10.1046/J.1365-2222.1999.00011.X
关键词: Bronchial hyperresponsiveness 、 Asthma 、 Eosinophil cationic protein 、 Immunology 、 Rhinovirus 、 Inflammation 、 Eosinophil 、 Respiratory virus 、 Common cold 、 Medicine
摘要: There is renewed interest in the role of respiratory virus infections pathogenesis asthma and development exacerbations pre-existing disease. This due to availability new molecular experimental tools. Circumstantial evidence points towards a potentially causative as well possibly protective effects certain viruses cause allergic during early childhood. In addition, it now has become clear that asthma, children adults, are mostly associated with infections, predominant common cold virus: rhinovirus. Careful human vitro vivo experiments have shown rhinovirus can stimulate bronchial epithelial cells produce pro-inflammatory chemokines cytokines, may activate cholinergic- or noncholinergic nerves, increase epithelial-derived nitric oxide synthesis, upregulate local ICAM-1 expression, lead nonspecific T-cell responses and/or virus-specific proliferation. Experimental patients demonstrate features exacerbation, such lower airway symptoms, variable airways obstruction, hyperresponsiveness, latter being eosinophil counts eosinophilic cationic protein levels induced sputum. suggests multiple cellular pathways be involved rhinovirus-induced exacerbations. It still unknown whether these mechanisms distinguishing characteristic asthma. Because limited inhaled steroids exacerbations, therapeutic interventions need developed based on increasing pathophysiological knowledge about