# HOST DEFENSE MECHANISM:  CONTROL OF SURGICAL INFECTION

> **NIH NIH R01** · UNIVERSITY OF CINCINNATI · 1989 · $471,800

## Abstract

The overall objective of this research is to improve host defense
mechanisms as a means for controlling infections in surgical patients.
This will be accomplished through several broadly specific aims:  1)
determination of the role of intestinal bacteria and/or endotoxin in the
hypermetabolic response following burn injury; 2) determination of the
optimal dietary composition for nutritional support of septic subjects; 3)
a study of the effect of burn and/or infection on the synthesis and release
of specific macrophage products and their effects on host defense; 4)
continuation of testing promising immunomodulators to determine their role
in improving resistance to infection with different bacteria in normal and
burned animal models with examination of the mechanism of action; 5)
examination of leukocyte subpopulations and surface receptors in burn
patients and normal individuals; 6) testing immunomodulators in single and
multiple combinations with or without standard antibiotic therapy in burned
animals receiving a chronic infectious challenge.  The standard nutritional
model in animals will involve placement of a gastrostomy tube approximately
one week prior to either burn injury or implantation of a bacterial laden
sponge entraped in a fibrin clot and implanted into the peritoneal cavity.
A clinical study will be done to determine the benefit of enteral feeding
immediately postburn.  Leukocyte subpopulations will be studied using flow
cytometry to detect the presence and density of specific surface receptors
and to define subpopulation-function interrelationships.  Both presently
available and newly developed monoclonal antibodies will be used in these
studies for detection in these surface markers.  Finally, alterations in
mediators produced by macrophages from animals after burn, sepsis or
immunomodulator treatment will be studied.  The expected result of the
proposed research will be that an entirely new diet will be formulated for
optimal nutritional support in subjects with severe bacterial infection,
new immunomodulators and combinations of immune modulators will be
identified which will prove more effective for preventing and treating
infection in the immunodepressed or infected subject than is now possible,
and a better understanding of the mechanism whereby host defense can be
improved will be obtained.

## Key facts

- **NIH application ID:** 3125328
- **Project number:** 5R01AI012936-13
- **Recipient organization:** UNIVERSITY OF CINCINNATI
- **SAM.gov UEI:** DZ4YCZ3QSPR5
- **Principal Investigator:** J. WESLEY ALEXANDER
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1989
- **Award amount:** $471,800
- **Award type:** 5
- **Project period:** 1979-05-01 → 1990-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3125328

## Citation

> US National Institutes of Health, RePORTER application 3125328, HOST DEFENSE MECHANISM:  CONTROL OF SURGICAL INFECTION (5R01AI012936-13). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3125328. Licensed CC0.

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