Analysis of TLR on systemic coronary disease by periodontopathic bacteria

本实验采用C3H/HeN小鼠（野生型）和C3H/HeJ小鼠（tlr4缺失型）对牙周病c菌诱导的全身性冠状动脉疾病进行分析。使用牙龈卟啉单胞菌381对i.p（腹膜）和i.n（鼻腔）感染进行攻击。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学研究。本研究的结论如下：1。tlr4缺陷C3H/HeJ小鼠在酪蛋白刺激或活的牙龈p .刺激后KC反应低。C3H/HeN和C3H/HeJ.3之间mcla依赖性超氧化物生成无显著差异。在HRP/ARP检测后，C3H/HeN和C3H/HeJ腹膜渗出PMNs均未产生oci。C3H/HeJ小鼠的TNF和KC产量明显低于C3H/HeN小鼠。与C3H/HeN小鼠相比，C3H/HeJ小鼠的TNF和KC生成水平显著降低。在感染早期，C3H/HeJ小鼠体内对牙龈卟啉单胞菌的清除比C3H/HeN小鼠明显延迟。C3H/HeJ小鼠在感染24 ~ 48 h后出现菌血症，而C3H/HeN小鼠仅出现肺内PMN积聚，未出现菌血症。

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.