Abstract

There is increasing evidence that vulnerability to pneumococcal pneumonia is mediated by the expression of adhesion receptors for bacteria on lower airway cells. A key bacterial adhesion receptor is the platelet-activating factor receptor (PAFR). In vitro and animal studies have shown that upregulation of PAFR increases vulnerability to infection and blocking PAFR and knockdown of PAFR attenuates infection. Blocking PAFR may therefore be a novel therapeutic strategy in acute and chronic airway infection.