[P1-88] Expression Levels of ICAM-1 and LFA-1 in Plasma and PBMC of Children with Febrile Seizures
Objective: To explore the neuroimmunomodulation mechanism of ICAM-1 and LFA-1 in children with febrile seizures (FS). Methods: 60 children with FS were divided into simple FS (SFS) group in 30 cases and complex FS (CFS) group in 30 cases, and control group of 30 health children was matched with regard to age and sex. Adopting enzyme-linked immunosorbentassay (ELISA) and flow cytometry (FCM), we measured the levels of ICAM-1 and LFA-1 contained in plasma and peripheral blood mononuclear cell (PBMC) of children with FS and control group. Results: The plasma levels of soluble ICAM-1 (sICAM-1) in SFS group [(21.54±11.09)ng/ml] and CFS group [(24.34±6.86)ng/ml] were significantly lower than that in the control group [(29.73±12.39)ng/ml] (P<0.05). The plasma soluble LFA-1 (sLFA-1) levels of CFS, SFS and control groups were (12.30±8.04), (12.09±8.83) and(9.51±8.07)ng/ml respectively, but there was no statistical difference between various groups (P>0.05). The PBMC levels of ICAM-1 were significantly higher in SFS group [(29.96±12.31)%] than those in CFS group [(22.50±8.19)%] and control group [(14.21±11.31)%] (P<0.05), at same time, there was significantly higher expression in CFS group than in control group (P<0.05). However, the expression levels of LFA-1 was different from the ICAM-1 in the surface of PBMC. Of the three groups, the highest LFA-1 level was the SFS group [(50.89±21.36)%], the lowest LFA-1 level was the CFS group [(34.35±11.45)%] and (41.39±16.30)% was the LFA-1 level of control group in PBMC. Significant difference was found in three groups (P<0.05). Conclusion: As a kind of costimulatory immunologic molecule under early stress, ICAM-1/LFA-1 participate in leukocytic adherence and cascade reaction of adherence, which results in overexcitation of neurons on base of unadapting to fever stress and induces convulsive seizures. The process of neuronal immunopathology in CFS patients is more complex than that in SFS patients. Therefore, a new idea of neuroprotective therapy may be found by inhibiting the activity of ICAM-1/LFA-1 adhesion in FS.