Analysis of TLR on systemic coronary disease by periodontopathic bacteria

本实验采用C3 H/HeN小鼠（野生型）和C3 H/HeJ小鼠（TLR 4缺陷型），以牙龈卟啉单胞菌（Porphyromonasgingivalis）381腹腔内和腹腔内感染牙周病菌，观察牙周病菌诱导的全身性冠状动脉病变。(in鼻）感染。感染后进行TNF或KC细胞因子产生、PMN功能、杀菌试验和免疫组织化学研究。本研究的主要结论如下：1. TLR 4缺陷型C3 H/HeJ小鼠在酪蛋白或活牙龈卟啉单胞菌刺激后表现出低KC反应。C3 H/HeN和C3 H/HeJ之间的MCLA依赖的超氧化物产生没有显著差异。经HRP/阿普检测，C3 H/HeN和C3 H/HeJ腹膜渗出液PMN在牙龈卟啉单胞菌刺激下均无OCI产生. C3 H/HeJ小鼠在腹腔注射时TNF和KC的产生水平显著低于C3 H/HeN小鼠. C3 H/HeJ小鼠在i.n.时TNF和KC的产生水平显著低于C3 H/HeN小鼠。挑战。C3 H/HeJ小鼠体内牙龈卟啉单胞菌感染早期的清除比C3 H/HeN小鼠延迟. C3 H/HeJ小鼠在i.n.感染模型，而C3 H/HeN小鼠只显示肺内PMN积聚，但没有菌血症。

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.