| Summary: | Abstract Expression of the platelet-activating factor receptor is upregulated in the respiratory epithelium of smokers and chronic obstructive pulmonary disease patients. We have recently determined that increased expression of PAFr correlates with higher levels of adhesion to human bronchial epithelial cells by non-typable Haemophilus influenzae and Streptococcus pneumoniae which are major bacterial pathogens in acute exacerbations of COPD. In addition, we found that a PAFr antagonist decreased the adhesion of both respiratory bacterial pathogens to non-cigarette exposure control levels. This highlights the possibility that epithelial receptors, that are upregulated in response to cigarette smoke, could be targeted to specifically block chronic bacterial infections of the lower respiratory tract. In this commentary, we explore the question of whether adhesion to a temporally-upregulated host receptor is a common event in chronic bacterial disease, and as such, could represent a putative therapeutic target for blocking infection by respiratory and other pathogens.
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