Platelet-activating factor-induced contraction of human isolated bronchus

In recent years, platelet-activating factor (PAF) has been strongly implicated as a mediator involved in asthma. In non-asthmatic subjects, aerosolized PAF has been shown to cause bronchoconstriction. The mechanism of this in vivo effect is unknown. We have previously shown that PAF causes a contraction of human isolated bronchus that varies in magnitude between patients, and within tissues from the same patient. To examine the possibility that this variability in contraction was secondary to PAF-induced release of mediators from inflammatory or epithelial cells within the tissue, we examined the relationship between contractile responses to PAF and the presence of inflammatory or epithelial cells. We studied eight tissues from five patients. Of the eight tissues, four contracted, whilst four failed to contract, to PAF (7 x 10(-7) M). After the contractile response to PAF had been assessed by observing changes in isometric tone in vitro, bronchial rings were examined histologically to enable the quantification of inflammatory cell numbers and intact epithelium. No significant correlation was observed between the magnitude of contractions and numbers of eosinophils, neutrophils, lymphocytes, plasma cells, total cells or percentage intact epithelium. We conclude that it is unlikely that the variability in response to PAF in human isolated airways is related to the variability in inflammatory cell numbers or to the presence of epithelium. Thus, the contraction induced by PAF is probably not mediated via the release of a secondary mediator from the particular cells examined in this study.

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