Ko Y H, Delannoy M, Pedersen P L
Department of Biological Chemistry, Johns Hopkins University, School of Medicine, Baltimore, MD 21205-2185, USA.
FEBS Lett. 1997 Mar 24;405(2):200-8. doi: 10.1016/s0014-5793(97)00189-0.
In order to understand how lungs of healthy people, unlike those of cystic fibrosis (CF) patients, are protected against bacterial infections such as Pseudomonas aeruginosa, the following three key findings were made. First, P. aeruginosa do not multiply when planted onto tracheal epithelial cells from healthy humans but do so profusely on cells from deltaF508 CF patients. Second, some bacteria bind, and gain entrance into CF cells, even at a physiological salt concentration (104 mM). Third, human tracheal epithelial cells express an approximately 4 kDa peptide (hTAP), which is known in its bovine form to exhibit bactericidal action against P. aeruginosa. A model is proposed depicting both how normal epithelial cells, in a first-line self defense mechanism, may be protected against bacterial infection and how this mechanism may fail during the initial stages of CF.
为了弄清楚健康人的肺部与囊性纤维化(CF)患者的肺部不同,是如何抵御诸如铜绿假单胞菌之类的细菌感染的,有以下三项关键发现。第一,将铜绿假单胞菌接种到健康人的气管上皮细胞上时不会繁殖,但接种到ΔF508 CF患者的细胞上时却会大量繁殖。第二,即使在生理盐浓度(104 mM)下,一些细菌也会结合并进入CF细胞。第三,人类气管上皮细胞表达一种约4 kDa的肽(hTAP),已知其牛源形式对铜绿假单胞菌具有杀菌作用。提出了一个模型,描述正常上皮细胞在一线自我防御机制中如何免受细菌感染,以及在CF初期该机制可能如何失效。