# CHEMOTATIC MECHANISMS IN NEONATAL BACTERIAL INFECTION

> **NIH NIH R01** · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · 1987 · $99,882

## Abstract

The newborn human infant is especially susceptible to bacterial infections
because of immature host defenses.  One of the most consistent defects in
the neonate's host defense system is a marked abnormality in
polymorphonuclear leukocyte chemotaxis.  Unfortunately, very little is
known about the pathogenesis of this developmental defect in cell
movement.  In studies carried out during the first two years of this grant,
we have shown that the PMNs from neonates fail to form polymerized, or F
actin, from gel actin following stimulation with chemoattractant; a process
which is essential in providing the contractile forces required for cell
movement.  Additional experiments indicate that the PMNs from neonates fail
to undergo critical changes in membrane potential following chemotactic
factor stimulation and develop lower concentrations of intracellular free
calcium.  The early cyclic adenosine 3'5' monophosphate (cAMP) response to
chemotactic factor stimulation is also blunted in the PMNs from neonates.
These results suggest that an abnormality in signal transduction may result
in the developmental abnormality in cell motility observed in the human
neonate.  Based on these rather exciting preliminary results, we wish to
attempt to define the exact mechanism(s) of the defect and attempt to
correct the abnormality.  Specifically, we will 1) determine if the rigid
cell membrane of the PMNs from neonates is preventing lateral mobility of
receptors and blunting or blocking signal transduction; 2) attempt to
define the reasons for, and significance of, the lack of changes in
membrane potential and the smaller increases in intracellular in free
intracellular calcium in the neonatal PMN; and 3) attempt to develop
pharmacologic regimens for correcting the chemotactic responsiveness of
PMNs from neonates.

## Key facts

- **NIH application ID:** 3128524
- **Project number:** 5R01AI019094-06
- **Recipient organization:** UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH
- **SAM.gov UEI:** LL8GLEVH6MG3
- **Principal Investigator:** HARRY R HILL
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $99,882
- **Award type:** 5
- **Project period:** 1982-09-01 → 1989-05-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3128524

## Citation

> US National Institutes of Health, RePORTER application 3128524, CHEMOTATIC MECHANISMS IN NEONATAL BACTERIAL INFECTION (5R01AI019094-06). Retrieved via MORVS 2026-10-26 from https://api.morvs.ai/grant/nih/3128524. Licensed CC0.

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