الفهرس 
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Abstract
We have investigated the effect of proinflammatory molecules known to act as rrning factors, such as the bacterial lipopolysaccharide (LPS) and plateletvating factor (PAF), on peripheral blood neutrophil functions. We also studied
tre mechanisms by which this priming state could alter the normal neutrophil Fysiologic response to a pathologic one capable of inducing some sort of tissue estruction that could happen in periodontal disease activities.
An in vitro model system of a blood vessel wall construct has been developed ivch consists of endothelial cell monolayer, a basement membrane, and a subrdothelial type 1 collagen . This model system allowed us to study the physioc gic and pathologic interactions that occur when a chemotacticaly-stimulated e.itrophils migrated through the layers of the blood vessel wall in a manner similiar to that of the postcapillary venules, the normal site of neutrophil extravasa: 1cm. The isolated neutrophils were cultured on the upper surface of the polycar:cnate microporous filter which has been previously overlaid with a type 1 :Alagen gel. The endothelial cells formed a confluent monolayer on the collagen mrthin 5 to 10 days. The movement of the primed and non-primed neutrophils has :een followed at the light and electron microscopic levels and their effects on the :ellular component and supporting collagen matrix evaluated . Other aspects of
-eutrophil-endothelial cell interaction have been investigated including the ex:ression of surface adhesion molecules and cytotoxicity of primed neutrophils on ndothelial cells.
from the results of this study, the following can be concluded :
1- Priming by LPS or PAF enhances superoxide production and degranulation while inhibiting neutrophil chemotaxis.
2- Priming inhibits neutrophil migration through the in vitro blood vessel wall construct.
3- Primed neutophils were accompanied by more cellular destruction and