Shoji Noriaki, Yoshida Atsushi, Yu Zhiqian, Endo Yasuo, Sasano Takashi
Department of Oral Diagnosis, Graduate School of Dentistry, Tohoku University, Seiryo-machi, Aoba-ku Sendai 980-8575, Japan.
Arch Oral Biol. 2006 Oct;51(10):856-60. doi: 10.1016/j.archoralbio.2006.04.004.
To examine the potential role of the histamine-forming enzyme, histidine decarboxylase (HDC), in oral inflammation and disease, we studied HDC activity in oral tissue after induction by bacterial agents. Following injection of E. coli-derived lipopolysaccharide (LPS) into mice, we measured the quantitative changes in HDC activity over time in dental pulp and gingiva. Oral tissue taken from individual mice was insufficient for detecting precise HDC activity, thus, we combined dental pulp or gingival tissues from four mice and assayed them over the course of 24 h. Our results indicate that LPS stimulated marked elevations of HDC activity in dental pulp and gingiva. This increase reached a maximum at 6 h after LPS injection and remained detectable at for least 24 h. Since mast cells are known to produce histamine through a difference mechanism than HDC induction, we compared LPS-induced HDC activity in dental pulp and gingiva to that in ear skin (a tissue rich in mast cells) and liver (a tissues lacking in mast cells). LPS also induced a marked increase in the HDC activity in liver and ear skin at 6 h after LPS injection. By contrast, saline injection had no effect on the HDC activity in any of the four tissues, although basal levels of HDC activity in ear skin was markedly higher than basal HDC activity in the other three kinds of tissues. Still, the relative increase in LPS-induced HDC activity in dental pulp and gingiva were much greater than that in ear skin. Since liver are devoid of mast cells and ear skin is considered the tissue richest in mast cells, the differences in HDC activity between tissues indicates that histamine induced by LPS may be produced by cells other than mast cells through another mechanism of action. These results also suggest that histamine produced in oral tissues in response to bacterial agents such as LPS could be involved in development of pulpitis or gingivitis (periodontitis), the most common diseases in the dental clinic, and that efforts to inhibit HDC activity, which elevates histamine levels in oral tissues, might offer the basis for novel treatment strategies.
为了研究组胺生成酶——组氨酸脱羧酶(HDC)在口腔炎症和疾病中的潜在作用,我们研究了细菌制剂诱导后口腔组织中的HDC活性。将大肠杆菌衍生的脂多糖(LPS)注射到小鼠体内后,我们测量了牙髓和牙龈中HDC活性随时间的定量变化。取自个体小鼠的口腔组织不足以检测精确的HDC活性,因此,我们将四只小鼠的牙髓或牙龈组织合并,并在24小时内对其进行检测。我们的结果表明,LPS刺激牙髓和牙龈中HDC活性显著升高。这种增加在LPS注射后6小时达到最大值,并至少在24小时内可检测到。由于已知肥大细胞通过与HDC诱导不同的机制产生组胺,我们将LPS诱导的牙髓和牙龈中的HDC活性与耳皮肤(富含肥大细胞的组织)和肝脏(缺乏肥大细胞的组织)中的活性进行了比较。LPS注射后6小时,LPS也诱导肝脏和耳皮肤中的HDC活性显著增加。相比之下,注射生理盐水对这四种组织中的HDC活性均无影响,尽管耳皮肤中HDC活性的基础水平明显高于其他三种组织中的基础HDC活性。不过,LPS诱导的牙髓和牙龈中HDC活性的相对增加远大于耳皮肤中的增加。由于肝脏中没有肥大细胞,而耳皮肤被认为是肥大细胞最丰富的组织,组织间HDC活性的差异表明,LPS诱导的组胺可能由肥大细胞以外的细胞通过另一种作用机制产生。这些结果还表明,口腔组织中响应LPS等细菌制剂产生的组胺可能参与牙髓炎或牙龈炎(牙周炎)的发展,这是牙科诊所最常见的疾病,并且抑制HDC活性(这会提高口腔组织中的组胺水平)的努力可能为新的治疗策略提供基础。