Abstract
NIF is a novel 41-kD glycoprotein from canine hookworm and potently inhibits CD 11/CD 18 dependent neutrophil adhesion in vitro, by binding to CD 11 b/CD 18. We examined the effects of NIF on neutrophil-dependent endothelial cell injury. Studies were made in bovine pulmonary microvessel endothelial monolayer and the injury was estimated as an increase of transendothelial 125I-albumin permeability.
Layering of neutrophils onto monolayer followed by activation of neutrophils with 500 nM of phorbol 12-myristate 13-acetate (PMA) increased the permeability (by 3-4 folds over control that is monolayers) .
Pretreatment of neutrophils with NIF completely protected the increase of permeability in a dose-dependent manner at 100 nM and above. Neutrophils pretreated with monoclonal antibody (mAb) IB 4, an anti-CD 18 mAb, also prevented the increase of permeability.
In contrast, pretreatment of neutrophil with OKM-1, a control anti-CD 11b mAb, did not affect the neutrophil-dependent permeability increase.
We conclude that NIF protects the neutrophil-dependent endothelial cell injury by preventing CD 18 dependent neutrophil activation.
