Secretory leukocyte protease inhibitor and its potential interactions with elastase and cathepsin B in gingival crevicular fluid and saliva from patients with chronic periodontitis
Secretory leukocyte protease inhibitor and its potential interactions with elastase and cathepsin B in gingival crevicular fluid and saliva from patients with chronic periodontitis
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DOI：
10.1111/j.1600-0765.2006.00891.x
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发表时间：
2006-10-01
影响因子：
3.5
通讯作者：
Eley, B. M.
中科院分区：
文献类型：
--
作者：
Cox, S. W.;Rodriguez-Gonzalez, E. M.;Eley, B. M.
背景与目的：弹性蛋白酶是由牙周病损的龈沟液（GCF）携带进入口腔的。我们的研究探讨了弹性蛋白酶活性的调节分泌性白细胞蛋白酶抑制剂（SLPI）和另一种GCF蛋白酶对这种保护性salivary component.Material和方法：全口唾液（WMS），腮腺唾液（PS）和GCF的可能行动，从19例牙周炎患者获得。使用肽底物测定活性弹性蛋白酶和组织蛋白酶B的浓度。采用酶联免疫吸附试验（ELISA）测定SLPI和α 1-蛋白酶抑制剂（α 1 PI）浓度。结果：GCF中弹性蛋白酶、组织蛋白酶B和α 1 PI的摩尔浓度均高于WMS，尤以PS为甚（p < 0.0002）。GCF SLPI浓度也高于WMS SLPI浓度（p < 0.05）。所有WMS组分均随GCF含量增加而增加，弹性蛋白酶和SLPI显著增加（p < 0.002）。GCF中α 1 PI浓度高于SLPI（p < 0.0002），而WMS中α 1 PI浓度与SLPI无显著性差异。GCF和WMS中SLPI和弹性蛋白酶水平呈负相关（p < 0.005）。在SLPI免疫印迹中，PS仅含有完整的14 kDa SLPI分子，而WMS也含有8 kDa片段。对于WMS，SLPI降解与组织蛋白酶B之间存在正相关性（p < 0.002）。温育的WMS单独或PS与GCF中存在的半胱氨酸蛋白酶激活剂引起SLPI免疫反应性转移到8 kDa.Conclusion：对于GCF，血清衍生的α 1 PI是主要的弹性蛋白酶抑制剂，但在WMS SLPI可能降低活性。发炎的牙龈炎可能是口腔中SLPI的额外来源，但此处该分子显然被GCF半胱氨酸蛋白酶（例如组织蛋白酶B）裂解。
Background and Objective: Elastase is carried into the oral cavity by gingival crevicular fluid (GCF) from periodontal lesions. Our study investigated the regulation of elastase activity by secretory leukocyte protease inhibitor (SLPI) and the possible action of another GCF protease on this protective salivary component.Material and Methods: Whole-mouth saliva (WMS), parotid saliva (PS) and GCF were obtained from 19 patients with periodontitis. The concentrations of active elastase and cathepsin B were determined using peptide substrates. SLPI and alpha 1-proteinase inhibitor (alpha 1PI) concentrations were determined using enzyme-linked immunosorbent assays (ELISAs). The molecular forms of SLPI were examined by immunoblotting.Results: The molar concentrations of elastase, cathepsin B and alpha 1PI were higher in GCF than in WMS and especially PS (p < 0.0002). The GCF SLPI concentrations were also higher than the WMS SLPI concentrations (p < 0.05). All WMS components increased with GCF content, significantly for elastase and SLPI (p < 0.002). In GCF, the concentration of alpha 1PI was higher than the concentration of SLPI (p < 0.0002), while there was no significant difference for WMS. SLPI and elastase levels in GCF and WMS were inversely related (p < 0.005). In SLPI immunoblots, PS contained only the intact 14-kDa molecule of SLPI, while WMS also contained an 8-kDa fragment. For WMS there was a positive correlation between SLPI degradation and cathepsin B (p < 0.002). Incubation of WMS alone or of PS with GCF in the presence of cysteine proteinase activators caused SLPI immunoreactivity to shift to 8 kDa.Conclusion: For GCF, serum-derived alpha 1PI is the major elastase inhibitor, but in WMS SLPI probably reduces activity. The inflamed gingivae can be an additional source of SLPI in the oral cavity, but here the molecule is apparently cleaved by GCF cysteine proteinases, such as cathepsin B.