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目的:比较脂多糖(LPS)诱导的内毒素血症BALB/c小鼠及重症联合免疫缺陷(SCID)小鼠炎症反应的差异。方法:建立LPS诱导的BALB/c小鼠和SCID小鼠内毒素血症模型,观察小鼠的存活率。分别于诱导前、诱导后3h、6h、12h,取小鼠的血清及诱导后12h小鼠的肝脏、肺脏,用全自动生化分析仪检测两种小鼠血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、尿素氮(BUN)水平;HE染色评价肝脏、肺脏的炎症病理改变;用流式细胞术微球阵列法检测两种小鼠血清TNF-α、IFN-γ、IL-6及MCP-1的水平。结果:(1)LPS诱导内毒素血症后,SCID小鼠于12～24h均死亡(8/8),BALB/c小鼠仅1只死亡(1/8)。(2)LPS诱导后12h,BALB/c小鼠及SCID小鼠血清ALT、AST、BUN的水平均明显升高(P<0.05),SCID小鼠前两项均高于BALB/c小鼠(P<0.05),但BUN两种小鼠无显著差异。(3)肺脏,肝脏炎症盲法的病理评分,SCID小鼠均高于BALB/c小鼠(P<0.05)。(4)SCID小鼠和BALB/c小鼠LPS诱导后3h、6h、12h,血清TNF-α,IFN-γ的水平,诱导后12h,IL-6,MCP-1的水平均显著升高(P<0.05),SCID小鼠明显高于BALB/c小鼠(P<0.05)。结论:LPS刺激SCID小鼠后,可分泌过量的炎性细胞因子,导致更严重的内毒素血症和脏器损伤,是造成小鼠死亡的重要原因。结果提示,缺乏适应性免疫应答细胞调控的情况下,异常增强的固有免疫应答,可能是危及机体生命的重症全身炎症反应综合征发生的重要原因。
OBJECTIVE: To compare the difference of inflammation in BALB / c mice and severe combined immunodeficiency (SCID) mice induced by lipopolysaccharide (LPS). Methods: LPS induced BALB / c mice and SCID mice endotoxemia model was established to observe the survival rate of mice. Serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (ALT) were measured in serum of mice and liver and lung of mice at 12h after induction, 3h, 6h, 12h after induction, (AST) and blood urea nitrogen (BUN) were measured. The pathological changes of liver and lung were evaluated by HE staining. The levels of serum TNF-α, IFN-γ, IL-6 and MCP were detected by flow cytometry -1 level. Results: (1) After LPS-induced endotoxemia, SCID mice died (8/8) in 12 to 24 hours and only 1 patient died (1/8) in BALB / c mice. (2) The levels of ALT, AST and BUN in serum of BALB / c mice and SCID mice were significantly increased at 12h after LPS induction (P <0.05), and the first two of SCID mice were significantly higher than that of BALB / c mice P <0.05), but no significant difference between BUN two mice. (3) The pathological score of lung and liver inflammation were higher in SCID mice than in BALB / c mice (P <0.05). (4) Serum levels of TNF-α and IFN-γ at 3h, 6h, 12h after induction of LPS in SCID mice and BALB / c mice significantly increased levels of IL-6 and MCP-1 at 12h after induction P <0.05). SCID mice were significantly higher than BALB / c mice (P <0.05). Conclusion: LPS stimulated SCID mice can secrete excessive inflammatory cytokines, leading to more serious endotoxemia and organ damage, which is an important cause of death in mice. The results suggest that in the absence of adaptive immune response to cellular regulation, an abnormally increased innate immune response may be an important cause of severe systemic inflammatory response syndrome that endangers life.