Integrin expression on neutrophils in a rabbit model of group B streptococcal meningitis

Products released by polymorphonuclear cells (PMNs) during an acute inflamm atory response can result in diffuse tissue injury. Integrins are cell surf ace adhesion proteins that play a pivotal role in inflammation by allowing PMNs to adhere to the endothelium and migrate through the extracellular mat rix. We examined the expression of beta(1) and beta(2) integrins on neutrop hils from blood and cerebrospinal fluid (CSF) in an animal model of Group B Streptococcal meningitis. We further evaluated whether integin expression correlates with pathophysiologic markers of central nervous system inflamma tion. Our data demonstrate that beta(1) and beta(2) integrin expression on circulating neutrophils does not significantly increase as a consequence of meningitis. In extravesated CSF neutrophils, a significant increase in exp ression of both beta(1) and beta(2) integrins is noted. Furthermore, a majo rity of the beta(1) integrins on extravesated neutrophils have undergone af finity modulation. Using regression analysis, we demonstrated that increasi ng beta(1) integrin expression correlates with decreasing CSF glucose conce ntration and serum/CSF glucose ratio. Regression analysis approached signif icance when CSF protein was compared to PMN beta(1) integrin expression. Po lymorphonuclear leukocytes beta(1) integrin expression also showed a direct correlation to myeloperoxidase activity in brain tissue. beta(2) expressio n on CSF PMNs did not correlate with these markers of inflammation/sequestr ation. These data demonstrate integrin expression on extravesated neutrophi ls markedly increases during meningitis and support a role for beta(1) inte grins on neutrophils in the pathophysiologic consequences of meningitis.