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目的探讨细胞间黏附因子-1(ICAM-1)及其配体淋巴细胞功能相关抗原-1(LFA-1)对热性惊厥(FS)患儿的神经免疫调节作用。方法2004-11—2006-12将武汉市儿童医院60例FS患儿分为单纯性FS(SFS)组30例和复杂性FS(CFS)组30例;对照组30例,为年龄和性别相匹配的同期体检健康儿童。采用双抗夹心ELISA法检测血浆可溶性ICAM-1/LFA-1水平,流式细胞术检测外周血单个核细胞(PBMC)表面ICAM-1/LFA-1的表达水平。结果SFS组和CFS组患儿血浆ICAM-1水平分别为(21.54±11.09)ng/mL和(24.34±6.86)ng/mL,均明显低于对照组(29.73±12.39)ng/mL儿童(P<0.05);3组血浆LFA-1水平从高到低依次为CFS组(12.30±8.04)ng/mL、SFS组(12.09±8.83)ng/mL和对照组(9.51±8.07)ng/mL,组间比较差异无统计学意义(P>0.05)。SFS组的PBMC表面ICAM-1表达水平为(29.96±12.31)%,明显高于CFS组(22.50±8.19)%及对照组(14.21±11.31)%儿童(P<0.05),CFS组的PBMC表面ICAM-1表达水平明显高于对照组儿童(P<0.05);而LFA-1在PBMC表面的表达水平则不同,3组比较,SFS组最高为(50.89±21.36)%,CFS组最低为(34.35±11.45)%,对照组为(41.39±16.30)%,组间比较差异有统计学意义。结论ICAM-1/LFA-1作为早期应激状态下的协同刺激信号免疫因子,参与白细胞黏附及其黏附级联反应,使大脑神经元在对热应激不适应基础上呈过度兴奋状态,诱导惊厥的发生。且CFS的神经免疫病理过程要比SFS相对复杂,抑制FS的ICAM-1/LFA-1黏附活动可能为其防治开辟新的途径。
Objective To investigate the neuroimmunological effects of intercellular adhesion molecule-1 (ICAM-1) and its ligand LFA-1 on children with febrile seizures (FS). Methods From November 2004 to December 2006, 60 children with FS in Wuhan Children’s Hospital were divided into 30 cases of simple FS (SFS) group and 30 cases of complicated FS (CFS) group. The control group consisted of 30 cases of age and sex Match the same period of physical examination of healthy children. Plasma soluble ICAM-1 / LFA-1 levels were measured by double-antibody sandwich ELISA. The expression of ICAM-1 / LFA-1 on peripheral blood mononuclear cells (PBMCs) was detected by flow cytometry. Results The levels of ICAM-1 in children with SFS and CFS were (21.54 ± 11.09) ng / mL and (24.34 ± 6.86) ng / mL, respectively, which were significantly lower than those in control group (29.73 ± 12.39) ng / mL <0.05). The levels of LFA-1 in three groups were (12.30 ± 8.04) ng / mL in CFS group, (12.09 ± 8.83) ng / mL in SFS group and 9.51 ± 8.07 ng / mL in control group There was no significant difference between the two groups (P> 0.05). The expression level of ICAM-1 on the surface of PBMC in SFS group was (29.96 ± 12.31)%, significantly higher than that in CFS group (22.50 ± 8.19%) and control group (14.21 ± 11.31)% (P <0.05) The expression level of ICAM-1 in PBMCs was significantly higher than that in control group (P <0.05), while the expression level of LFA-1 was different in PBMCs (50.89 ± 21.36)% in SFS group and 34.35 ± 11.45)%, and the control group was (41.39 ± 16.30)%, the difference between the two groups was statistically significant. CONCLUSION: ICAM-1 / LFA-1, as a costimulatory signal in the early stage of stress, participates in the leukocyte adhesion and its adhesion cascade, which makes the neurons in the brain hyperexcitably excited and induces Occurrence of convulsions. The pathological process of neuroimmunopathology of CFS is more complex than that of SFS. Inhibiting ICAM-1 / LFA-1 adhesion activity of FS may open up a new way for its prevention and treatment.