Nakata Setsuko, Yasui Kozo, Nakamura Tomohiko, Kubota Noriko, Baba Atsushi
Department of Pediatrics, Shinshu University School of Medicine, Nagano, Japan.
Neonatology. 2007;91(2):127-33. doi: 10.1159/000097130. Epub 2006 Nov 20.
BACKGROUND/AIMS: Human pulmonary alveolar epithelial (A549) cells release interleukin-8 (IL-8) on stimulation by lipopolysaccharide (LPS) and alpha-toxin. We hypothesised that the perfluorocarbons (PFCs), perflubron and FC-84, would block stimulation of A549 cells by these toxins.
The levels of IL-8 production in A549 cells were measured following exposure to toxins for 24 h with or without PFC. The amount of IL-8 released from A549 cells was measured by enzyme-linked immunosorbent assay, and the level of IL-8 mRNA was measured by real-time RT-PCR.
When stimulated with LPS or alpha-toxin, IL-8 release from A549 cells increased. There were no significant differences in level of IL-8 release between cells pre-incubated for 24 h with or without PFC after toxin stimulation for 24 h. When PFC was administered along with LPS stimulation, the level of IL-8 release was decreased (LPS control, 1,398 +/- 110 pg/well; FC-84, 686 +/- 50 pg/well; perflubron, 749 +/- 137 pg/well; p < 0.05). Levels of IL-8 mRNA expression were significantly higher with than without LPS, and those with LPS and perflubron were significantly lower than those with LPS alone.
The results show that PFCs block stimulation of A549 cells by LPS or alpha-toxin. PFC may be useful clinically in treatment of pulmonary inflammation in the alveolar space.
背景/目的:人肺泡上皮(A549)细胞在受到脂多糖(LPS)和α毒素刺激时会释放白细胞介素-8(IL-8)。我们假设全氟化碳(PFCs)、全氟溴辛烷和FC-84会阻断这些毒素对A549细胞的刺激。
在有或没有PFC的情况下,将A549细胞暴露于毒素24小时后,测量细胞中IL-8的产生水平。通过酶联免疫吸附测定法测量A549细胞释放的IL-8量,并通过实时逆转录聚合酶链反应测量IL-8 mRNA的水平。
用LPS或α毒素刺激时,A549细胞释放的IL-8增加。毒素刺激24小时后,预先孵育24小时有或没有PFC的细胞之间IL-8释放水平没有显著差异。当PFC与LPS刺激同时给予时,IL-8释放水平降低(LPS对照组,1398±110 pg/孔;FC-84,686±50 pg/孔;全氟溴辛烷,749±137 pg/孔;p<0.05)。有LPS时IL-8 mRNA表达水平显著高于无LPS时,有LPS和全氟溴辛烷时显著低于单独有LPS时。
结果表明PFCs可阻断LPS或α毒素对A549细胞的刺激。PFC在临床上可能对治疗肺泡腔内的肺部炎症有用。