Regueiro V, Campos M A, Morey P, Sauleda J, Agustí A G N, Garmendia J, Bengoechea J A
Program Infection and Immunity, Fundació Caubet-CIMERA Illes Balears, Recinto Hospital Joan March, Carretera Sóller Km 12, 07110 Bunyola, Spain.
Eur Respir J. 2009 Feb;33(2):273-81. doi: 10.1183/09031936.00087708. Epub 2008 Nov 14.
Lipopolysaccharide-binding protein (LBP) and CD14 contribute to the recognition of pathogens by cells, which triggers the activation of defence responses. Smoking is a risk factor for the development of chronic obstructive pulmonary disease (COPD) and respiratory infections. The current authors theorised that levels of LBP and CD14 in the lungs of smokers would be higher than those in the lungs of never-smokers. These elevated levels could affect host responses upon infection. LBP, soluble CD14 (sCD14) and interleukin (IL)-8 were detected by ELISA. Nuclear factor (NF)-kappaB, p38 and the inhibitor IkappaBalpha were studied by immunoassays. Gene expression was assessed by RT-PCR. Bronchoalveolar lavage levels of LBP and CD14 were significantly higher in smokers and COPD patients than in never-smokers, whereas levels of both proteins were not significantly different between smokers and COPD patients. IL-6, IL-1beta and cigarette smoke condensate induced the expression of LBP and CD14 by airway epithelial cells. LBP and sCD14 inhibited the nontypeable Haemophilus influenzae (NTHi)-dependent secretion of IL-8 and the activation of NF-kappaB and p38 mitogen-activated protein kinase signalling pathways but they increased the internalisation of NTHi by airway epithelial cells. Thus, in the inflamed airways of smokers both proteins could contribute to inhibit bacteria-dependent cellular activation without compromising the internalisation of pathogens by airway cells.
脂多糖结合蛋白（LBP）和CD14有助于细胞识别病原体，从而触发防御反应的激活。吸烟是慢性阻塞性肺疾病（COPD）和呼吸道感染发生的危险因素。本文作者推测，吸烟者肺部的LBP和CD14水平会高于从不吸烟者肺部的水平。这些升高的水平可能会影响感染时的宿主反应。通过酶联免疫吸附测定（ELISA）检测LBP、可溶性CD14（sCD14）和白细胞介素（IL）-8。通过免疫测定研究核因子（NF）-κB、p38和抑制剂IκBα。通过逆转录聚合酶链反应（RT-PCR）评估基因表达。吸烟者和COPD患者支气管肺泡灌洗中的LBP和CD14水平显著高于从不吸烟者，而吸烟者和COPD患者之间这两种蛋白的水平没有显著差异。IL-6、IL-1β和香烟烟雾冷凝物诱导气道上皮细胞表达LBP和CD14。LBP和sCD14抑制非分型流感嗜血杆菌（NTHi）依赖的IL-8分泌以及NF-κB和p38丝裂原活化蛋白激酶信号通路的激活，但它们增加了气道上皮细胞对NTHi的内化。因此，在吸烟者发炎的气道中，这两种蛋白都可能有助于抑制细菌依赖性细胞激活，而不会影响气道细胞对病原体的内化。
