中华生物医学工程杂志
中華生物醫學工程雜誌
중화생물의학공정잡지
CHINESE JOURNAL OF BIOMEDICAL ENGINEERING
2011年
4期
359-362
,共4页
黄书炜%周传华%吕翠媚%刘启乐%冯炽光%李炳灿%周伟
黃書煒%週傳華%呂翠媚%劉啟樂%馮熾光%李炳燦%週偉
황서위%주전화%려취미%류계악%풍치광%리병찬%주위
脓毒症%多器官功能障碍综合征%Toll样受体%肿瘤坏死因子%白介素6
膿毒癥%多器官功能障礙綜閤徵%Toll樣受體%腫瘤壞死因子%白介素6
농독증%다기관공능장애종합정%Toll양수체%종류배사인자%백개소6
Sepsis%Multy-organ dysfunction syndrome%Toll-like receptors%Tumor necrosis factor α%Interleukin 6
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。
目的 探討膿毒癥嬰幼兒Toll樣信號傳導途徑相關因子改變的臨床意義。方法 選取廣東省肇慶市耑州區婦幼保健院和廣州市兒童醫院2009年6月至2011年3月收治膿毒癥患兒20例（膿毒癥組），重癥膿毒癥感染性休剋及多器官功能障礙綜閤徵患兒20例（嚴重膿毒癥組），以同時期20例健康嬰幼兒為健康對照組。用流式細胞儀檢測外週血單箇覈細胞(PBMC)錶麵Toll樣受體2(TLR2)、TLR4的錶達情況；酶聯免疫吸附法檢測血漿中前炎性細胞因子腫瘤壞死因子α(TNF-α)、白細胞介素6(IL-6)的濃度變化。結果膿毒癥組和嚴重膿毒癥組嬰幼兒外週血PBMC錶麵TLR2、TLR4的錶達暘性率比健康對照組均明顯增高[(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]；嚴重膿毒癥組嬰幼兒PBMC錶麵TLR2、TLR4的錶達明顯高于膿毒癥組(P＜0.01)。與健康對照組比較，膿毒癥組血漿TNF-α和IL-6水平均明顯增高，且嚴重膿毒癥組較膿毒癥組升高更加明顯(P＜0.01)。結論 TLR2和TLR4可能共同參與瞭嬰幼兒膿毒癥時機體對病原微生物的識彆，激活TLR信號通路。嬰幼兒膿毒癥時TLR2和TLR4可能介導瞭血清前炎性因子TNF-α,IL-6的產生和釋放。
목적 탐토농독증영유인Toll양신호전도도경상관인자개변적림상의의。방법 선취광동성조경시단주구부유보건원화엄주시인동의원2009년6월지2011년3월수치농독증환인20례（농독증조），중증농독증감염성휴극급다기관공능장애종합정환인20례（엄중농독증조），이동시기20례건강영유인위건강대조조。용류식세포의검측외주혈단개핵세포(PBMC)표면Toll양수체2(TLR2)、TLR4적표체정황；매련면역흡부법검측혈장중전염성세포인자종류배사인자α(TNF-α)、백세포개소6(IL-6)적농도변화。결과농독증조화엄중농독증조영유인외주혈PBMC표면TLR2、TLR4적표체양성솔비건강대조조균명현증고[(52.48±27.37)％화（80.56.±42.95）％비(15.63±9.28)％；(26.58±14.26)％화(49.32±23.74)％비(2.84±2.0r7)％；균P＜0.01]；엄중농독증조영유인PBMC표면TLR2、TLR4적표체명현고우농독증조(P＜0.01)。여건강대조조비교，농독증조혈장TNF-α화IL-6수평균명현증고，차엄중농독증조교농독증조승고경가명현(P＜0.01)。결론 TLR2화TLR4가능공동삼여료영유인농독증시궤체대병원미생물적식별，격활TLR신호통로。영유인농독증시TLR2화TLR4가능개도료혈청전염성인자TNF-α,IL-6적산생화석방。
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.
