Suri Reetika, Mallia Patrick, Martin Joanne E, Footitt Joseph, Zhu Jie, Trujillo-Torralbo Maria-Belen, Johnston Sebastian L, Grigg Jonathan
Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK.
Airway Disease Infection Section, National Heart and Lung Institute, Imperial College London, London W2 1PG, UK.
Respir Med. 2014 Jun;108(6):898-904. doi: 10.1016/j.rmed.2014.03.003. Epub 2014 Mar 18.
Bacteria expressing phosphorylcholine (ChoP) co-opt host-expressed platelet-activating factor receptor (PAFR) to adhere to lower airway cells. Cigarette smoke and rhinovirus (RV) infection upregulate PAFR-dependent bacterial adhesion to airway cells in vitro, and in healthy adults smoking increases the proportion of PAFR positive bronchial epithelial cells. To date the effect of chronic obstructive pulmonary disease (COPD) on smoke-induced PAFR is unknown. We therefore sought to test the hypothesis that bronchial PAFR mRNA expression is increased in smokers with chronic obstructive pulmonary disease (COPD), and further increases after RV infection.
Endobronchial biopsies were obtained by fibreoptic bronchoscopy from healthy non-smokers, smokers without airway obstruction, and smokers with COPD, before and after infection with rhinovirus (RV) serotype 16. Endobronchial PAFR mRNA expression was assessed by quantitative PCR and expressed as a ratio of glyceraldehyde-3-phosphate dehydrogenase. The distribution of PAFR was assessed by immunohistochemistry.
Baseline PAFR mRNA expression was increased (p < 0.05) in smokers (n = 16), and smokers with COPD (n = 14) compared with non-smokers (n = 18). In RV16 infected subjects there was no increase in PAFR mRNA expression in either non-smokers (n = 9), smokers (n = 8), or smokers with COPD (n = 7). PAFR immunoreactivity in all 3 groups was predominately restricted to the bronchial epithelium and submucosal glands.
Endobronchial PAFR mRNA is increased in both smokers without airway obstruction and smokers with COPD. We found preliminary evidence that RV16 infection does not increase PAFR mRNA expression in either smokers or smokers with COPD.
表达磷酸胆碱（ChoP）的细菌利用宿主表达的血小板活化因子受体（PAFR）黏附于下呼吸道细胞。香烟烟雾和鼻病毒（RV）感染在体外上调PAFR依赖性细菌对气道细胞的黏附，并且在健康成年人中，吸烟会增加PAFR阳性支气管上皮细胞的比例。迄今为止，慢性阻塞性肺疾病（COPD）对烟雾诱导的PAFR的影响尚不清楚。因此，我们试图验证以下假设：慢性阻塞性肺疾病（COPD）吸烟者的支气管PAFR mRNA表达增加，并且在RV感染后进一步增加。
通过纤维支气管镜从健康非吸烟者、无气道阻塞的吸烟者以及患有COPD的吸烟者中获取支气管活检组织，在感染16型鼻病毒（RV）之前和之后进行检测。通过定量PCR评估支气管PAFR mRNA表达，并表示为甘油醛-3-磷酸脱氢酶的比值。通过免疫组织化学评估PAFR的分布。
与非吸烟者（n = 18）相比，吸烟者（n = 16）和患有COPD的吸烟者（n = 14）的基线PAFR mRNA表达增加（p < 0.05）。在RV16感染的受试者中，非吸烟者（n = 9）、吸烟者（n = 8）或患有COPD的吸烟者（n = 7）的PAFR mRNA表达均未增加。所有3组中的PAFR免疫反应性主要局限于支气管上皮和黏膜下腺。
无气道阻塞的吸烟者和患有COPD的吸烟者的支气管PAFR mRNA均增加。我们发现初步证据表明，RV16感染不会增加吸烟者或患有COPD的吸烟者的PAFR mRNA表达。
