Bronchial epithelial cell-cytokine interactions in airway inflammation

Abstract

A variety of cytokine bronchial cell interactions may play an important role in normal host defense as well as in the pathogenesis of inflammatory airway disorders such as asthma, cystic fibrosis, acute and chronic bronchitis, and bronchiectasis. First, airway epithelial cells may participate in local cytokine networks by synthesizing interleukins, chemokines, colony stimulating factors and growth factors in response to inflammatory mediators. Bronchial epithelial cell derived cytokines may thereby amplify ongoing inflammatory processes via the recruitment and activation of specific subsets of inflammatory cells, as well as by prolonging their survival in the airway microenvironment. Second, airway epithelial cells can initiate inflammatory cascades by generating cytokines in direct response to viral and bacterial products, noxious gases, and sensitizing chemicals. Third, airway epithelial cells represent targets for paracrine acting cytokines, which may then modulate bronchial epithelial cell functions. Finally, airway epithelial cells may modulate ongoing inflammatory events in the airway microenvironment via the shedding of soluble TNF receptors. Cytokine-bronchial epithelial cell interactions represent an important mechanism by which inflammatory events in the airway microenvironment can be regulated and represent potential targets for novel anti-inflammatory therapies in airway disorders.