目的：探讨肿瘤坏死因子-α(TNF-α) 对热性惊厥(FS) 患儿外周血单个核细胞（PBMC）细胞间黏附分子-1(ICAM-1) 及配体淋巴细胞功能相关抗原-1(LFA-1) 表达的影响。方法：16例FS患儿随机分为FS对照组和TNF-α干预组。TNF-α干预组采用1.0 ng/mL 的TNF-α进行干预。对照组16例，为年龄和性别相匹配的同期体检健康儿童。进行外周血PBMC培养。流式细胞仪检测PBMC表面ICAM-1 和 LFA-1的表达。结果：FS 对照组在体外培养的PBMC表面ICAM-1和LFA-1表达水平分别为(20±9)% 和(43±16)%，明显高于正常对照组［(14±7)%，(30±16)%］（P＜0.05）；TNF-α干预组的PBMC表面ICAM-1表达水平［(27±11)%］明显高于FS对照组(P＜0.05)，LFA-1表达［（52±21）%］较FS对照组有增高趋势，但差异无统计学意义。结论：炎症介质TNF-α刺激可使FS患儿的LFA-1 和 ICAM-1表达上调。
Abstract
OBJECTIVE: To study the effects of TNF-α on ICAM-1 and LFA-1 expression in peripheral blood mononuclear cells (PBMC) of children with febrile seizures (FS). METHODS: Sixteen children with FS and 16 age- and gender-matched healthy children were enrolled. The samples of PBMC from FS children were randomized into two groups with or without TNF-α treatment (TNF-α concentration 1.0 ng/mL). PBMC were purified and cultured with a conventional method in vitro. The expression of ICAM-1 and LFA-1 in PBMC was determined by flow cytometry (FCM). RESULTS: ICAM-1［(20±9)% vs (14±7)%)］and LFA-1［(43±16)% vs (30±16)%］expression in PBMC in the untreated FS group was significantly higher than that in the normal control group (P<0.05). Compared with the untreated FS group, the treatment with TNF-α remarkably increased the ICAM-1 expression［(27±11)%］(P<0.05). PBMC LFA-1 expression［(52±21)%］in the TNF-α-treated group was higher than that in the untreated FS group, although there were no statistical differences between the two groups. CONCLUSIONS: TNF-α treatment may increase LFA-1 and ICAM-1 expression in PBMC of children with FS.
关键词
肿瘤坏死因子-α /
热性惊厥 /
ICAM-1 /
LFA-1 /
外周血单个核细胞 /
儿童
Key words
TNF-α /
Febrile seizure /
ICAM-1 /
LFA-1 /
Peripheral blood mononuclear cell /
Child
{{custom_sec.title}}
{{custom_sec.title}}
{{custom_sec.content}}
参考文献
［1］沈晓明，王卫平. 儿科学［M］. 第7版. 北京：人民卫生出版社，2000: 400-402.
［2］Tsoyi K, Jang HJ. PTEN differentially regulates expressions of ICAM-1 and VCAM-1 through P13K/AKT/GSK-3β/GATA-6 signaling pathways in TNF-α-activated human endothelial cells［J］. Atherosclerosis, 2010, 213(1): 115-121.
［3］Librizzi L, Regondi MC, Pastori C, Frigerio S, Frassoni C, de Cutis M. Expression of adhesion factors induced by epileptiform activity in the endothelium of the isolated guinea pig brain in vitro［J］. Epilepsia, 2007, 48(4):743-751.
［4］Kumar B, Kalita J, Misra UK. Febrile seizure［J］. J Indian Med Assoc, 2010, 108(7): 441-442.
［5］Gaffuri B, Vigano P, Nozza A, Gornati G, DT Blasio AM, Vignali M. Expression of intercellular adhesion molecule-1 messenger ribonucleic acid and protein in human term placental cells and its modulation by pro-inflammatory cytokines (interleukin-1 beta and tumor necrosis factor alpha)［J］. Biol Repord, 1998, 58(4):1003-1008.
［6］Petzold T, Orr AW, Hahn C. Focal adhesion Kinase modulates activation of NF-kappaB by flow in endothelial cells［J］. Am J Physiol Cell Physiol, 2009, 297(4):C814-822.
［7］Rahman A, Anwar KN, Malik AB. Protein kinase C-zeta mediates TNF-alpha-induced ICAM-1 gene transcription in endothelial cells［J］. Am J Physiol Cell Physiol, 2000, 279(4): C906-C914.
［8］刘智胜，孙丹，姚辉，康世秀，何彩英，胡家胜，等. 热性惊厥患儿血浆和外周血单个核细胞表面ICAM-1/LFA-1的表达水平［J］. 中国实用儿科杂志, 2007, 22(11):826-829.
PDF(930 KB)
