Interleukin-1 and interleukin-8 in nicotine- and lipopolysaccharide-exposed gingival keratinocyte cultures
Interleukin-1 and interleukin-8 in nicotine- and lipopolysaccharide-exposed gingival keratinocyte cultures
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DOI：
10.1111/j.1600-0765.2009.01262.x
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发表时间：
2010-08-01
影响因子：
3.5
通讯作者：
Dawson, D. V.
中科院分区：
文献类型：
--
作者：
Johnson, G. K.;Guthmiller, J. M.;Dawson, D. V.
背景和目的：在吸烟者和无烟者中，烟草使用都与牙周破坏增加有关。牙周角质形成细胞是第一个与微生物和烟草成分接触的细胞，在对这些物质的先天免疫反应中起着关键作用。本研究旨在探讨尼古丁和细菌脂多糖(LPS)单独及联合作用对牙周角质形成细胞分泌白介素1α(IL-1α)和白介素8(IL-8)的影响。材料和方法：10例健康非吸烟受试者建立牙周角质形成细胞培养体系。用1mM或1 mM尼古丁和/或10mUg/mLE或牙龈卟啉单胞菌脂多糖刺激细胞24 h。结果：与未经处理的培养物相比，1 mM尼古丁可促进IL-1α的产生(p<；0.001)，而大肠杆菌和牙龈假单胞菌可促进IL-8的产生(p=0.0014和p=0.0232)。尼古丁和脂多糖的组合产生了最高的细胞因子数量。在1 mM尼古丁和脂多糖暴露后，IL-1α和IL-8的量显著高于未经处理的培养物(p<；0.001)。与对照组相比，IL-8对0.1mM尼古丁与大肠杆菌或牙龈假单胞菌脂多糖的联合培养也有反应(p<；0.0001和p=0.0029)。结论：尼古丁和脂多糖对牙周角质形成细胞产生IL-1和IL-8有不同程度的调节作用。联合治疗倾向于进一步提高细胞因子的产生，这可能与吸烟者牙周炎的进展有关。
Background and Objective:Tobacco use is associated with increased periodontal destruction in both cigarette smokers and smokeless tobacco users. Gingival keratinocytes are the first cells in contact with microbial and tobacco components and play a key role in the innate immune response to these agents. The objective of this study was to evaluate the effect of nicotine and bacterial lipopolysaccharide (LPS) alone and in combination on gingival keratinocyte production of interleukin-1 alpha (IL-1 alpha) and interleukin-8 (IL-8).Material and Methods:Gingival keratinocyte cultures were established from 10 healthy, non-tobacco-using subjects. The cells were stimulated for 24 h with 1 mu m or 1 mm nicotine and/or 10 mu g/mL Escherichia coli or Porphyromonas gingivalis LPS. Interleukin-1 alpha and IL-8 proteins were quantified using ELISAs.Results:Compared with untreated cultures, 1 mm nicotine stimulated production of IL-1 alpha (p < 0.001); E. coli and P. gingivalis LPS increased IL-8 production (p = 0.0014 and p = 0.0232, respectively). A combination of nicotine and LPS produced the highest cytokine quantities. Amounts of IL-1 alpha and IL-8 following 1 mm nicotine and LPS exposure were significantly greater than in untreated cultures (p < 0.001). Interleukin-8 was also responsive to 0.1 mu m nicotine combined with E. coli or P. gingivalis LPS compared with control cultures (p < 0.0001 and p = 0.0029, respectively). Both cytokines tended to be elevated following the combined treatment relative to nicotine or LPS treatment alone.Conclusion:These results demonstrate that nicotine and LPS differentially regulate IL-1 and IL-8 production by gingival keratinocytes. Combined treatment tended to elevate cytokine production further, which may have implications for the progression of periodontitis in tobacco users.