Kido Jun-ichi, Hayashi Noriko, Kataoka Masatoshi, Nagata Toshihiko
Department of Periodontology and Endodontology, Tokushima University School of Dentistry, Tokushima, Japan.
J Periodontol. 2003 Dec;74(12):1719-24. doi: 10.1902/jop.2003.74.12.1719.
Calprotectin is a major cytosolic protein of monocytes, granulocytes, and epithelial cells. It is known that calprotectin is released in inflammatory tissues and detected in gingival crevicular fluid (GCF) of periodontitis patients at high levels. The origin of calprotectin in GCF and its regulation in periodontal disease are unknown. In this study, we investigated the distribution of calprotectin in gingival tissue with inflammation and the induction of calprotectin release from human monocytes by lipopolysaccharide of Porphyromonas gingivalis (P-LPS), tumor necrosis factor-alpha (TNF-alpha), or interleukin-1beta (IL-1beta).
Gingival tissues were obtained from a healthy donor and a periodontitis patient and calprotectin in gingival tissues was examined by immunohistochemical staining. Monocytes were isolated from the peripheral blood of healthy donors and cultured with P-LPS, TNF-alpha or IL-1beta for 30 minutes to 4 hours. The content of calprotectin in the cell and medium fractions was determined by enzyme-linked immunosorbent assay (ELISA).
Calprotectin was markedly detected at the epithelial and adjacent connective tissue with many inflammatory cells in the gingival tissue from the periodontitis patient. P-LPS increased calprotectin release from monocytes to the maximum level after 30 minutes of treatment and its level was elevated to about 2- to 3-fold of the control level in a dose-dependent manner (1 to 1,000 ng/ml). When the effect of TNF-alpha and IL-1beta on calprotectin release was investigated, calprotectin release significantly increased to about 2.2- and 1.5-fold that of the control level, respectively.
These results demonstrate that calprotectin release from monocytes is induced by P-LPS, TNF-alpha, and IL-1beta, which in turn, cause and aggravate periodontal disease.
钙卫蛋白是单核细胞、粒细胞和上皮细胞的一种主要胞质蛋白。已知钙卫蛋白在炎症组织中释放，并且在牙周炎患者的龈沟液（GCF）中可检测到高水平。GCF中钙卫蛋白的来源及其在牙周疾病中的调节尚不清楚。在本研究中，我们调查了钙卫蛋白在炎症牙龈组织中的分布，以及牙龈卟啉单胞菌脂多糖（P-LPS）、肿瘤坏死因子-α（TNF-α）或白细胞介素-1β（IL-1β）对人单核细胞释放钙卫蛋白的诱导作用。
从一名健康供体和一名牙周炎患者获取牙龈组织，通过免疫组织化学染色检测牙龈组织中的钙卫蛋白。从健康供体的外周血中分离单核细胞，并用P-LPS、TNF-α或IL-1β培养30分钟至4小时。通过酶联免疫吸附测定（ELISA）测定细胞和培养基组分中钙卫蛋白的含量。
在来自牙周炎患者的牙龈组织中，上皮及相邻结缔组织处有许多炎症细胞，可明显检测到钙卫蛋白。P-LPS处理30分钟后使单核细胞释放钙卫蛋白达到最高水平，且其水平以剂量依赖方式（1至1000 ng/ml）升高至对照水平的约2至3倍。当研究TNF-α和IL-1β对钙卫蛋白释放的影响时，钙卫蛋白释放分别显著增加至对照水平的约2.2倍和1.5倍。
这些结果表明，P-LPS、TNF-α和IL-1β可诱导单核细胞释放钙卫蛋白，进而导致和加重牙周疾病。
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