# PREMATURE LABOR, ENDOTOXEMIA AND CYTOKINE MECHANISMS

> **NIH NIH K11** · UNIVERSITY OF MISSOURI-COLUMBIA · 1994 · $89,100

## Abstract

The single greatest cause of mortality and morbidity in newborn infants is
premature birth.  Although the pathogenic factors responsible for preterm
parturition are unknown, recent studies indicate that endotoxin from
bacterial infection can provoke the release of tumor necrosis factor
(TNFalpha), interleukin 1 (IL-1beta), and platelet activating factor (PAF)
from the decidua and are then projected to cause premature labor through
some unknown mechanism.  We propose to test two hypotheses:  that TNFalpha,
IL-1beta and PAF directly alter myometrial contractile function and that
endotoxemia alters uterine contractile characteristics.  Contractile
effects of TNFalpha, IL-1beta and PAF will be examined singly and in
combination with known agonists in uterine effects of TNFalpha, PAF and
IL-1beta are altered by known receptor antagonists, determine if
gestational age alters susceptibility to TNFalpha, PAF and/or IL-1beta, and
determine the role of the decidua in mediating the effects of these
substances on myometrial contractile mechanisms.  E. coli endotoxemia will
be induced to determine E. coli endotoxemia alters contractile responses of
pregnant uterus to TNFalpha, IL-1beta, oxytocin and PGF2alpha, and to
determine if endotoxin is necessary to "prime" the gravid uterus and/or its
decidua for expression of the myometrial effects of TNFalpha, and IL-1beta.

These studies are designed to provide insight into cellular mechanisms
responsible for the relationship of bacterial infection to premature labor.
An understanding of these mechanisms could lead to the development of
methods that would reduce premature births, as well as to a better
comprehension of basic physiologic mechanisms that govern uterine function
and parturition.

## Key facts

- **NIH application ID:** 2194416
- **Project number:** 5K11HD000947-04
- **Recipient organization:** UNIVERSITY OF MISSOURI-COLUMBIA
- **SAM.gov UEI:** SZPJL5ZRCLF4
- **Principal Investigator:** SCOTT W SNYDER
- **Activity code:** K11 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1994
- **Award amount:** $89,100
- **Award type:** 5
- **Project period:** 1991-06-01 → 1994-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/2194416

## Citation

> US National Institutes of Health, RePORTER application 2194416, PREMATURE LABOR, ENDOTOXEMIA AND CYTOKINE MECHANISMS (5K11HD000947-04). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/2194416. Licensed CC0.

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