TNF-alpha release in monocytes after exposure to calcium hydroxide treated Escherichia coli LPS
TNF-alpha release in monocytes after exposure to calcium hydroxide treated Escherichia coli LPS
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DOI：
10.1111/j.1365-2591.1997.tb00690.x
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发表时间：
1997-05-01
影响因子：
5
通讯作者：
Trope, M
中科院分区：
文献类型：
--
作者：
Barthel, CR;Levin, LG;Trope, M
脂多糖（LPS）是革兰氏阴性厌氧菌的细胞壁成分，与感染根管引起的根尖周病的发病机制有关。氢氧化钙[Ca（OH）（2）]已被证明是治疗此类感染的有效药物，可降低根管内的微生物滴度。已提出Ca（OH）（2）的治疗效果也可能是LPS直接灭活的结果。本研究的目的是研究Ca（OH）（2）是否能降低或消除大肠杆菌LPS的毒性。四种浓度的E.将范围为1-1000 ng/ml的大肠杆菌LPS与25 mg Ca（OH）（2）或单独的无菌水孵育，一式两份。对照由不含LPS的Ca（OH）（2）或仅无菌水组成。通过梯度离心从外周血收集单核细胞，并铺板至特定密度。将贴壁单核细胞在37 ℃、5%CO2、含10%自体血清的M199培养基中孵育4天。在第5天将不同的LPS溶液加入到威尔斯孔中。4小时后，收集上清液并使用商业ELISA试剂盒定量测定TNF-α。采用方差分析进行统计学分析。结果表明，Ca（OH）（2）能消除E. coli LPS刺激外周血单核细胞产生TNF-α（P
Lipopolysaccharide (LPS), a cell wall component of Gram negative anaerobic bacteria, has been implicated in the pathogenesis of periapical disease resulting from infected root canals. Calcium hydroxide [Ca(OH)(2)] has been shown to be an effective medicament in such infections, reducing the microbial titre within the canal, It has been proposed that the therapeutic effect of Ca(OH)(2) may also be the result of direct inactivation of LPS. The aim of this study was to investigate whether the toxic potential of an Escherichia col LPS could be reduced or eliminated by Ca(OH)(2). Four concentrations of E. coli LPS ranging from 1-1000 ng/ml sterile water were incubated in duplicate either with 25 mg Ca(OH)(2) or sterile water alone. Controls consisted of Ca(OH)(2) without LPS or sterile water only. Monocytes were collected from peripheral blood by centrifuging through a gradient and plated to a specific density. Adherent monocytes were incubated for 4 days at 37 degrees C with 5% CO2 in M199 medium with 10% autologous serum. The different LPS solutions were added to the wells on day 5. After 4 h the supernatants were collected and quantitatively assayed for TNF-alpha using a commercial ELISA kit. Statistical analysis was performed with ANOVA. Results indicated that Ca(OH)(2) is able to eliminate the ability of an E. coli LPS to stimulate TNF-alpha production in peripheral blood monocytes (P