Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary, University of London, 4 Newark Street, London E1 2AT, UK.
Thorax. 2012 Sep;67(9):840-1. doi: 10.1136/thoraxjnl-2012-202206. Epub 2012 Jul 16.
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.
越来越多的证据表明,对肺炎球菌性肺炎的易感性是由下呼吸道细胞上细菌黏附受体的表达所介导的。一个关键的细菌黏附受体是血小板激活因子受体(PAFR)。体外和动物研究表明,PAFR 的上调增加了感染的易感性,而阻断 PAFR 和 PAFR 的敲低则减弱了感染。因此,阻断 PAFR 可能是急性和慢性气道感染的一种新的治疗策略。