This statement is also supported by impressive protective effects through adhesion-promoting neutrophil receptor blockade using a neutralizing anti-CD18 antibody, neutrophil depletion, and neutrophil apoptosis induction (76–78), each eliciting massive neutropenia within the perivascular and subarachnoid space, the site of pneumococcal infection in meningitis, thus blunting inflammatory immune activity therein. Here, ITGB2 is linked to pneumococcal infection.