在MRSA系统性感染模型中Pam3CSK4预处理降低小鼠肾组织的炎症反应
发布时间：2018-11-15 13:49
【摘要】：目的:在耐甲氧西林金葡菌(MRSA)系统性感染模型中,观察低剂量TLR2激动剂Pam3CSK4预处理对小鼠肾组织中炎症反应的影响并初步探讨其机制。方法:于感染前48 h、24 h对BALB/c小鼠行尾静脉注射Pam3CSK4(10μg/100μl/只);2×10~7CFU/只MRSA经静脉感染小鼠,ELISA和荧光实时定量PCR(Q-PCR)检测细胞因子水平,Q-PCR检测TLR2、IRAKs等相对表达量,Western blot检测NF-κB p65磷酸化、IRAK-M及A20表达。结果:与对照组相比,预处理组在感染6 h后肾组织中TNF-α、IL-6、IL-1β、CCL3和IFN-γ含量显著减少,i NOS表达量降低,IL-10和TGF-β表达量增高,TLR2表达下降;处理组肾组织在感染12 h后IRAK-1表达无明显增加,而IRAK-M表达量显著增加;Western blot结果显示Pam3CSK4预处理组NF-κBp65磷酸化降低,IRAK-M表达明显增高。结论:Pam3CSK4预处理降低MRSA系统性感染小鼠肾组织的炎症反应,这可能与诱导IRAK-M表达相关。
[Abstract]:Aim: to investigate the effect of low-dose TLR2 agonist Pam3CSK4 preconditioning on inflammatory reaction in mouse kidney tissue in a systemic infection model of methicillin-resistant Staphylococcus aureus (MRSA) and to explore its mechanism. Methods: Pam3CSK4 (10 渭 g / 100 渭 l / mouse) was injected into the tail vein of BALB/c mice 48 h before infection. 2 脳 10~7CFU/ mice were infected with MRSA via vein. The levels of cytokines were detected by ELISA and real-time quantitative PCR (Q-PCR), and NF- 魏 B p65 phosphorylation, IRAK-M and A20 expression were detected by NF- 魏 B p65 phosphorylation, NF- 魏 B p65 phosphorylation and IRAK-M and A20 expression by Q-PCR. Results: compared with the control group, the contents of TNF- 伪, IL-6,IL-1 尾, CCL3 and IFN- 纬 in renal tissue of preconditioning group decreased significantly after 6 h infection, the expression of, i NOS decreased, IL-10 and TGF- 尾 increased, and TLR2 decreased. The expression of IRAK-1 in renal tissue of the treated group did not increase significantly at 12 h after infection, but the expression of IRAK-M increased significantly in the; Western blot group. The results showed that the phosphorylation of NF- 魏 Bp65 decreased and the expression of IRAK-M increased significantly in the Pam3CSK4 pretreatment group. Conclusion: Pam3CSK4 preconditioning can reduce the inflammatory response in renal tissue of MRSA systemic infection mice, which may be related to the induction of IRAK-M expression.
【作者单位】： 南方医科大学基础医学院免疫学教研室;
【基金】：国家自然科学基金(31270980)资助
【分类号】：R-332;R515
[Abstract]:Aim: to investigate the effect of low-dose TLR2 agonist Pam3CSK4 preconditioning on inflammatory reaction in mouse kidney tissue in a systemic infection model of methicillin-resistant Staphylococcus aureus (MRSA) and to explore its mechanism. Methods: Pam3CSK4 (10 渭 g / 100 渭 l / mouse) was injected into the tail vein of BALB/c mice 48 h before infection. 2 脳 10~7CFU/ mice were infected with MRSA via vein. The levels of cytokines were detected by ELISA and real-time quantitative PCR (Q-PCR), and NF- 魏 B p65 phosphorylation, IRAK-M and A20 expression were detected by NF- 魏 B p65 phosphorylation, NF- 魏 B p65 phosphorylation and IRAK-M and A20 expression by Q-PCR. Results: compared with the control group, the contents of TNF- 伪, IL-6,IL-1 尾, CCL3 and IFN- 纬 in renal tissue of preconditioning group decreased significantly after 6 h infection, the expression of, i NOS decreased, IL-10 and TGF- 尾 increased, and TLR2 decreased. The expression of IRAK-1 in renal tissue of the treated group did not increase significantly at 12 h after infection, but the expression of IRAK-M increased significantly in the; Western blot group. The results showed that the phosphorylation of NF- 魏 Bp65 decreased and the expression of IRAK-M increased significantly in the Pam3CSK4 pretreatment group. Conclusion: Pam3CSK4 preconditioning can reduce the inflammatory response in renal tissue of MRSA systemic infection mice, which may be related to the induction of IRAK-M expression.
【作者单位】： 南方医科大学基础医学院免疫学教研室;
【基金】：国家自然科学基金(31270980)资助
【分类号】：R-332;R515
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