Objective: To investigate whether bacterial DNA involving in the pathogenesis of systemic inflammatory response syndrome (SIRS) and possible mechanism. Methods: Escherichia coli DNA (EC DNA) was extracted from Escheri...Objective: To investigate whether bacterial DNA involving in the pathogenesis of systemic inflammatory response syndrome (SIRS) and possible mechanism. Methods: Escherichia coli DNA (EC DNA) was extracted from Escherichia coli 25922 with alkaline lysis method. The mice mortality was observed after EC DNA was injected into mice via caudal vein. The changes of serum TNF-α and IL-6 levels in rats were measured with ELISA after rats were given EC DNA. Calf thymus DNA and lipopolysaccharide (LPS) were used as the control, respectively. Results: EC DNA led mice to death with notable dose-effect relationship (LD50=11.51 mg/kg), but CT DNA didn't. The peak level of TNF-αwas lower in EC DNA group than in LPS group (P＜0. 05), though the former reaching the peak I h earlier than the latter. However, they had coordinate ability to induce IL-6 release in rats, and no significant difference was seen in serum IL-6 peak level between 2 groups. Conclusion: EC DNA leads mice to death, and induces the increases of serum TNF-αand IL-6 levels in rats. EC DNA has the effect equal to LPS in inducing SIRS by triggering cytokines cascade.展开更多
基金National Natural Science Foundation of China (No. 30070299)
文摘Objective: To investigate whether bacterial DNA involving in the pathogenesis of systemic inflammatory response syndrome (SIRS) and possible mechanism. Methods: Escherichia coli DNA (EC DNA) was extracted from Escherichia coli 25922 with alkaline lysis method. The mice mortality was observed after EC DNA was injected into mice via caudal vein. The changes of serum TNF-α and IL-6 levels in rats were measured with ELISA after rats were given EC DNA. Calf thymus DNA and lipopolysaccharide (LPS) were used as the control, respectively. Results: EC DNA led mice to death with notable dose-effect relationship (LD50=11.51 mg/kg), but CT DNA didn't. The peak level of TNF-αwas lower in EC DNA group than in LPS group (P＜0. 05), though the former reaching the peak I h earlier than the latter. However, they had coordinate ability to induce IL-6 release in rats, and no significant difference was seen in serum IL-6 peak level between 2 groups. Conclusion: EC DNA leads mice to death, and induces the increases of serum TNF-αand IL-6 levels in rats. EC DNA has the effect equal to LPS in inducing SIRS by triggering cytokines cascade.
