【摘要】：目的:在耐甲氧西林金葡菌(MRSA)系統(tǒng)性感染模型中,觀察低劑量TLR2激動劑Pam3CSK4預處理對小鼠腎組織中炎癥反應的影響并初步探討其機制。方法:于感染前48 h、24 h對BALB/c小鼠行尾靜脈注射Pam3CSK4(10μg/100μl/只);2×10~7CFU/只MRSA經(jīng)靜脈感染小鼠,ELISA和熒光實時定量PCR(Q-PCR)檢測細胞因子水平,Q-PCR檢測TLR2、IRAKs等相對表達量,Western blot檢測NF-κB p65磷酸化、IRAK-M及A20表達。結(jié)果:與對照組相比,預處理組在感染6 h后腎組織中TNF-α、IL-6、IL-1β、CCL3和IFN-γ含量顯著減少,i NOS表達量降低,IL-10和TGF-β表達量增高,TLR2表達下降;處理組腎組織在感染12 h后IRAK-1表達無明顯增加,而IRAK-M表達量顯著增加;Western blot結(jié)果顯示Pam3CSK4預處理組NF-κBp65磷酸化降低,IRAK-M表達明顯增高。結(jié)論:Pam3CSK4預處理降低MRSA系統(tǒng)性感染小鼠腎組織的炎癥反應,這可能與誘導IRAK-M表達相關(guān)。
[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- 偽, IL-6,IL-1 尾, CCL3 and IFN- 緯 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.
【作者單位】： 南方醫(yī)科大學基礎醫(yī)學院免疫學教研室;
【基金】：國家自然科學基金(31270980)資助
【分類號】：R-332;R515

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