Bacterial endotoxins are important modulators of septic shock. We have examined for the first time the pathway of LPS action on neutrophils in blood. This pathway involves a plasma binding protein and a cell surface receptor CD14. We have shown that LPS can act directly upon the neutrophil in blood without the production of inflammatory mediators by other cell types. These studies set the stage for detailed mechanistic evaluation of the action of inflammatory mediators and regulators in physiological systems. LPS causes the modulation of important adhesive proteins on leukocyte-selectins and integrins which alter the ability of neutrophils to recognize one another and alter their compartmentation in the circulation. Ongoing studies are aimed at defining the relationship between the expression of adhesion molecules and neutrophil physiology.

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
Biotechnology Resource Grants (P41)
Project #
5P41RR001315-14
Application #
5223194
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
14
Fiscal Year
1996
Total Cost
Indirect Cost
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