Prostaglandin E-2 and interleukin-1 concentrations in nicotine-exposed oral keratinocyte cultures
Prostaglandin E-2 and interleukin-1 concentrations in nicotine-exposed oral keratinocyte cultures
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DOI：
10.1111/j.1600-0765.1997.tb00557.x
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发表时间：
1997-07-01
影响因子：
3.5
通讯作者：
Organ, CC
中科院分区：
文献类型：
--
作者：
Johnson, GK;Organ, CC
口腔角质形成细胞是与烟草成分接触的第一批细胞，能够产生各种炎症介质，包括PGE（2）和IL-1。本研究的目的是检测尼古丁暴露的口腔角质形成细胞培养物中PGE（2）和IL-1的浓度。牙龈角质形成细胞培养建立从健康牙龈组织从7个主题。将培养物分成4组，暴露于无血清培养基（对照）、0.1 μ M、10 μ M或1 mM尼古丁4、24或48 h。使用酶联免疫吸附测定法，定量测定培养上清液中的PGE（2）和IL-1 α;还测定裂解细胞中的IL-1 α和IL-1 β。重复测量方差分析用于确定随时间和治疗的显著差异。尼古丁暴露在任何给定的时间段内都没有显著改变PGE（2）水平;然而，PGE（2）的数量随着时间的推移显著下降（p= 0.0001）。在24和48小时，来自1 mM尼古丁暴露细胞的裂解物中的IL-1 α浓度显著（p < 0.01）高于所有其他处理的裂解物。在培养物中，白细胞介素-1 α的量也随时间显著下降（p= 0.037）。在24和48 h时，在1 mM处理的细胞中，白细胞介素-1 β浓度升高，尽管不显著。细胞活力、质量和计数不受尼古丁处理的影响;这些参数随时间显著增加（p < 0.005）。总之，尼古丁处理显著增加了培养的角质形成细胞中IL-1 α的浓度;然而，PGE（2）的合成没有改变。由于IL-1在组织对损伤的反应中起着重要作用，角质形成细胞产生的IL-1升高可能与烟草诱导的病变有关。
Oral keratinocytes are the first cells in contact with tobacco components and are capable of producing various inflammatory mediators, including PGE(2) and IL-1. The purpose of this study was to examine PGE(2) and IL-1 concentrations in nicotine-exposed oral keratinocyte cultures. Gingival keratinocyte cultures were established from healthy gingival tissues obtained from 7 subjects. Cultures were divided into 4 groups exposed to serum free medium (control), 0.1 mu M, 10 mu M or 1 mM nicotine for 4, 24 or 48 h. Using enzyme-linked immunosorbent assays, PGE(2) and IL-1 alpha were quantified in culture supernatants; IL-1 alpha and beta were also measured in lysed cells. A repeated measures analysis of variance was used to identify significant differences over time and treatment. Nicotine exposure did not significantly alter PGE(2) levels at any given time period; however, PGE(2) quantities declined significantly (p= 0.0001) over time. At both 24 and 48 h, IL-1 alpha concentrations in lysates from 1 mM nicotine-exposed cells were significantly (p < 0.01) greater than those for all other treatments. Interleukin-1 alpha quantities also declined significantly (p= 0.037) over time in the cultures. Interleukin-1 beta concentrations were elevated, albeit not significantly, in the 1 mM treated cells at 24 and 48 h. Cell viability, mass and counts were not affected by nicotine treatment; these parameters increased significantly (p < 0.005) over time. In summary, nicotine treatment significantly increased IL-1 alpha concentrations in cultured keratinocytes; however, PGE(2) synthesis was not altered. Elevated IL-1 production by keratinocytes may have implications in tobacco-induced lesions, given the central role IL-1 plays in tissue response to injury.