脓毒症婴幼儿Toll样信号传导途径相关因子改变的临床意义

目的 探讨脓毒症婴幼儿Toll样信号传导途径相关因子改变的临床意义。方法 选取广东省肇庆市端州区妇幼保健院和广州市儿童医院2009年6月至2011年3月收治脓毒症患儿20例（脓毒症组），重症脓毒症感染性休克及多器官功能障碍综合征患儿20例（严重脓毒症组），以同时期20例健康婴幼儿为健康对照组。用流式细胞仪检测外周血单个核细胞(PBMC)表面Toll样受体2(TLR2)、TLR4的表达情况；酶联免疫吸附法检测血浆中前炎性细胞因子肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)的浓度变化。结果脓毒症组和严重脓毒症组婴幼儿外周血PBMC表面TLR2、TLR4的表达阳性率比健康对照组均明显增高[(52.48±27.37)％和（80.56.±42.95）％比(15.63±9.28)％；(26.58±14.26)％和(49.32±23.74)％比(2.84±2.0r7)％；均P＜0.01]；严重脓毒症组婴幼儿PBMC表面TLR2、TLR4的表达明显高于脓毒症组(P＜0.01)。与健康对照组比较，脓毒症组血浆TNF-α和IL-6水平均明显增高，且严重脓毒症组较脓毒症组升高更加明显(P＜0.01)。结论 TLR2和TLR4可能共同参与了婴幼儿脓毒症时机体对病原微生物的识别，激活TLR信号通路。婴幼儿脓毒症时TLR2和TLR4可能介导了血清前炎性因子TNF-α,IL-6的产生和释放。

Clinical significance of alteration in factors associated with Toll-like receptor signaling pathway in infants with sepsis

Objective To investigate the clinical significance of alteration in factors associated with Toll-like receptor signaling pathway in infants with sepsis. Methods Twenty infants with sepsis (sepsis group) and another 20 with severe septic shock and multi-organ dysfunction syndrome (severe sepsis group) admitted to Duanzhou Women and Children Hospital in Zhaoqing and Guangzhou Women and Children Hospital between June 2009 and March 2011 were included in this study. A contemporary cohort of 20 healthy infants were set as control group. The expression of Toll- like receptor2 (TLR2) and receptor4 (TLR4) on peripheral blood mononuclear cells (PBMC) was examined with flow cytometry, and the plasma levels of tumor necrotizing factor alpha (TNF-α) and IL-6 with ELISA. Results The sepsis group and severe sepsis group showed significantly higher positive rates of TLR2 and TLR4 expression on PBMCs as compared with the control group[(52.48±27.37)％ and (80.56±42.95)％ vs (15.63±9.28)％; (26.58±14.26)％ and (49.32±23.74)％ vs (2.84±2.07)％; all P＜0.01]. The levels of TLR2 and TLR4 expression on PBMC were higher in severe sepsis group than those in sepsis group (P＜0.01). Compared with control group,the plasma pro-inflammatory cytokines TNF-α and IL-6 were significantly elevated in sepsis group and even higher in the severe sepsis group (P＜0.01). Conclusion In infants with sepsis, TLR2 and TLR4 may be involved in the pathogenic microbes and activation of TLR signaling pathway, and may also mediate production and release of serum pro-inflammatory factors, such as TNF-α and IL- 6.