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Articles in PresS, published online ahead of print October 10, 2001
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00196.2001
Submitted on May 14, 2001
Accepted on October 4, 2001
1 Pediatrics and Steele Memorial Children's Research Center, University of Arizona, Tucson, Arizona, USA; Cell Biology & Anatomy, University of Arizona, Tucson, Arizona, USA
2 Pediatrics and Steele Memorial Children's Research Center, University of Arizona, Tucson, Arizona, USA
3 Microbiology & Immunology, University of Arizona, Tucson, Arizona, USA
4 Cell Biology & Anatomy, University of Arizona, Tucson, Arizona, USA; Pediatrics and Steele Memorial Children's Research Center, University of Arizona, Tucson, Arizona, USA
* To whom correspondence should be addressed. E-mail: dvorakb{at}peds.arizona.edu.
Necrotizing enterocolitis (NEC) is the most common gastrointestinal disease of prematurely born infants. Maternal milk plays an important protective role against NEC development and is the major source of epidermal growth factor (EGF) for neonates. The aim of this study was to examine the effect of orally administered EGF on the incidence of NEC in a neonatal rat model. Newborn rats were artificially fed either with growth factor-free rat milk substitute (RMS) or RMS supplemented with 500 ng/ml of EGF (RMS+EGF). Experimental NEC was induced by exposure to asphyxia and cold stress. Development of NEC was evaluated by gross and histological scoring of damage in the ileum. Ileal EGF-receptor (EGF-R), EGF and transforming growth factor-alpha (TGF-
) mRNA expression was assessed by reverse-transcription competitive-PCR and the EGF-R was localized by immunohistochemistry. EGF supplementation of formula reduced the incidence and severity of NEC in rats (NEC, 13/16 RMS vs. 4/13 RMS+EGF). Ileal EGF-R mRNA expression was markedly increased in the RMS group compared to RMS+EGF. Enhanced EGF-R expression in the RMS group was localized predominantly in the epithelial cells of injured ileum. These data suggest a new potential therapeutic approach for the prevention and treatment of NEC.
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