Analysis of TLR on systemic coronary disease by periodontopathic bacteria

本实验用C3H/HEN小鼠(野生型)和C3H/HeJ(TLR4缺陷型)小鼠分析牙周病细菌所致的系统性冠脉病变。(在腹膜中)和I.N.(在鼻部)感染。感染后，进行肿瘤坏死因子或KC细胞因子的产生、中性粒细胞功能、杀菌实验和免疫组织学检测。本研究的结论如下：1.TLR4基因缺陷的C3H/HeJ小鼠在酪蛋白或活体牙龈假单胞菌刺激下表现出低的KC反应。C3 H/HEN和C3 H/HeJ.3细胞MCLA依赖的超氧化物生成无显著差异。经HRP/ARP检测后，C3H/HEN和C3H/HEJ腹膜渗出液的PMN在牙周炎杆菌的刺激下均不产生OCI。C3H/HeJ小鼠在腹腔注射时产生的肿瘤坏死因子和KC显著低于C3H/HEN小鼠。5.挑战。C3H/HeJ小鼠在iN时产生的肿瘤坏死因子和KC显著低于C3H/HEN小鼠。6.挑战。在感染早期，C3H/HeJ小鼠体内牙龈假单胞菌的清除较C3H/HEN小鼠延迟。C3H/HeJ小鼠在腹腔注射24~48小时后出现菌血症。感染模型，但C3H/HEN小鼠仅见PMN在肺内蓄积，未见菌血症。

In this experiments, C3H/HeN mice (wild type) and C3H/HeJ (TLR4-deficient type) were used for analysis of Periodontopathi cbacteria induced systemic coronary disease.Porphyromonas gingivalis 381 were used to challenge i.p. (in peritoneal) and i.n. (in nasal) infection. After infection, TNF or KC cytokine production, PMN function, bactericidal assay, and immunohistological study were done. The conclusions in this study was follows ;1. TLR 4 deficient C3H/HeJ mice showed low KC response after stimulation of casein or live P.gingivalis.2. MCLA-dependent super oxide production was no significant difference between C3H/HeN and C3H/HeJ.3. Following HRP/ARP assay, there were no OCI-production from both C3H/HeN and C3H/HeJ peritoneal exudates PMNs with stimulation of P.gingivalis.4. C3H/HeJ mice showed the significant lower level of TNF and KC production than C3H/HeN mice at i.p. challenge.5. C3H/HeJ mice showed the significant lower level of TNF and KC production than C3H/HeN mice at i.n. challenge.6. C3H/HeJ mice showed delay clearance of P.gingivalis in vivo than C3H/HeN mice at early phase of infection.7. C3H/HeJ mice showed bacteriemia after 24〜48 hours in i.n. infection model, but C3H/HeN mice only showed PMN accumulation in lung but no bacteriemia.