Adhesion molecule levels in serum and cerebrospinal fluid in children with bacterial meningitis and sepsis

Background: Adhesion molecules play a role in leukocyte recruitment during central nervous system (CNS) inflammation. Aim: This study was designed to compare serum, cerebrospinal fluid (CSF) concentrations of adhesion molecules in children with meningitis and sepsis, and to evaluate their sources. Setting: This study was carried out at Pediatric Department, King Abdulaziz University Hospital from January 2007 to June 2008. Design: Serum and CSF samples were collected on admission from meningitis (n = 40), sepsis ( n = 20) patients, and sera from controls ( n = 20). Materials and Methods: Endothelial (E), leukocyte (L), platelet (P) selectins intercellular cell adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecules-1 (VCAM-1) were measured using ELISA. Statistics: ANOVA and Spearman's correlations were used. Adhesion molecules with albumin concentration were estimated in CSF/serum to calculate concentration quotients. Results: In meningitis, serum sE-, sL-, sP-selectins sICAM-1, sVCAM-1 levels were higher than controls. Compared to sepsis, serum sE- selectin, sL- selectin, sVCAM-1, CSF- sL- selectin, CSF- sVCAM-1, VCAM-1 ratio and index were higher, while serum sP-selectin was lower than meningitis. sE- selectin ratio, CSF sICAM-1 were higher in meningitis with positive than negative culture. The sE- selectin index was higher in meningitis with neurological complication than those without it. In meningitis, correlation was found between CSF protein and CSF white blood cell counts (WBCs), CSF sICAM-1, CSF sVCAM-1 and between CSF sE-selectin and CSF sICAM-1. Conclusions: This study supports the role of adhesion molecules especially sL-selectin, sVCAM- 1 in meningitis and suggests further research to determine their use as biomarkers for meningitis and use of their antagonists as therapeutic for CNS inflammation. The presence of discrepancy of CSF/serum ratios for molecules of same molecular weight suggest intrathecal shedding in addition to diffusion through the blood-CSF barrier.