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Updated: Jul 13, 2026
05:39
A Neonatal BALB/c Mouse Model of Necrotizing Enterocolitis
Published on: November 30, 2021
The central role of PAF in necrotizing enterocolitis development
K Muguruma1, P W Gray, L W Tjoelker
1Department of Biochemistry, Cecil H. & Ida Green Center for Reproductive Biology Sciences, University of Texas Southwestern Medical Center at Dallas 75235-9051, USA.
Advances in Experimental Medicine and Biology
|January 1, 1997
Summary
Necrotizing enterocolitis (NEC) is linked to high platelet-activating factor (PAF) synthesis in newborns. Glucocorticoids may prevent NEC by increasing PAF inactivation and decreasing its synthesis, highlighting PAF
Area of Science:
- Biochemistry
- Neonatal Medicine
- Immunology
Background:
- Neonatal intestine susceptibility to necrosis.
- Platelet-activating factor (PAF) role in NEC development.
Purpose of the Study:
- Investigate neonatal intestine's susceptibility to NEC.
- Determine the critical role of PAF in NEC development.
- Elucidate the mechanisms of glucocorticoid action in NEC prevention.
Main Methods:
- Assessed acetyltransferase activity in neonatal intestinal tissue.
- Examined the effect of dexamethasone on PAF synthesis and inactivation pathways.
- Reviewed studies on recombinant PAF-acetylhydrolase in NEC prevention.
Main Results:
- Neonatal intestinal tissue exhibits high PAF synthesis capacity.
- Glucocorticoids may prevent NEC by increasing PAF inactivation and decreasing synthesis.
- Recombinant PAF-acetylhydrolase effectively prevents NEC, supporting PAF's central role.
Conclusions:
- High PAF biosynthetic activity in the neonatal intestine explains its susceptibility to NEC.
- Glucocorticoids likely prevent NEC through modulation of PAF metabolism.
- PAF plays a critical role in the pathogenesis of NEC.
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