# HOST DEFENSE MECHANISMS--CONTROL OF SURGICAL INFECTION

> **NIH NIH R01** · UNIVERSITY OF CINCINNATI · 1993 · $481,430

## Abstract

The long term objective of this grant since its inception has been to
improve host defense mechanisms as a means for controlling infections
and, thus, reduce morbidity and mortality in surgical patients.  After
definition of the abnormalities of host defense that occurred during
injury and infection, concepts of nutritional pharmacology were used to
develop diets using animal models which, in appropriate controlled
clinical trials, have resulted in a 20% reduction in hospital stay and
a 60 to 70 percent reduction in the incidence of post operative and post
traumatic infections.  Animal studies of early enteral feeding after
traumatic injury also lead to use in severely injured patients with a
highly significant reduction in infections in controlled clinical trials.
The success of these studies has more narrowly focused recent
investigations to the interactions of nutrition, gut function and sepsis.
It is now clear that translocation of microbes and their products is a
frequent occurrence in both laboratory animals and man.  Translocation
occurs very rapidly and triggers activation of cytokine, complement and
eicosanoid pathways in a regulated and orderly manner resulting in
inflammatory processes locally and in distant organs.  The magnitude or
severity of translocation is associated directly with overall mortality
and indirectly with length of survival in animals.  Treatments which
improve the barrier function to translocation consistently improved
survival in injured animals, and conversely, treatment which decreases
the gut barrier function increases mortality.  Gut barrier function may,
therefore, play an important role in a wide variety of diseases.  The
hypothesis that will be tested ultimately will be that control or
prevention of translocation in critically ill patients will improve
outcome as measured by a decrease in infectious complications, a decrease
in the incidence of the "septic syndrome", a reduction in hospital stay,
and, perhaps, an improvement in survival.

The specific aims of the present study are:  1) to develop improved tests
for the measurement of translocation of microbes and their products, 2)
to further delineate the mechanisms whereby microbial translocation
occurs, 3) to develop optimal therapeutic regimens for the prevention of
translocation, and, 4) to further delineate the pathophysiologic
consequences of microbial translocation.

## Key facts

- **NIH application ID:** 3125324
- **Project number:** 2R01AI012936-17
- **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:** 1993
- **Award amount:** $481,430
- **Award type:** 2
- **Project period:** 1979-05-01 → 1997-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3125324

## Citation

> US National Institutes of Health, RePORTER application 3125324, HOST DEFENSE MECHANISMS--CONTROL OF SURGICAL INFECTION (2R01AI012936-17). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3125324. Licensed CC0.

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