Studies suggest that the production of endogenous anti-inflammatory agents during sepsis reduces host defense and predisposes to subsequent infection. Whether such a state of immunosuppression during sepsis actually exists or is reversible with the administration of proinflammatory agents is unclear. However, use of recombinant granu- locyte colony stimulating factor (G-CSF) to augment host defense following the onset of sepsis in critically ill patients has been proposed. Using a rat model, we plan to determine whether an initial episode of infection and sepsis augments the host defense effects of G- CSF during a subsequent episode.

Agency
National Institute of Health (NIH)
Institute
Clinical Center (CLC)
Type
Intramural Research (Z01)
Project #
1Z01CL000184-03
Application #
6289412
Study Section
Special Emphasis Panel (CCM)
Project Start
Project End
Budget Start
Budget End
Support Year
3
Fiscal Year
1999
Total Cost
Indirect Cost
Name
Clinical Center
Department
Type
DUNS #
City
State
Country
United States
Zip Code