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Infection and Immunity, September 1999, p. 4787-4793, Vol. 67, No. 9
Department of Veterans Affairs Medical
Center, East Orange,1 and Departments of
Surgery2 and Anatomy, Cell Biology
and Injury Sciences,3 University of Medicine and
Dentistry of New Jersey, and Graduate School of Biomedical
Sciences,4 Newark, New Jersey
Received 19 January 1999/Returned for modification 4 March
1999/Accepted 27 May 1999
Multicellular organisms utilize a battery of extracellular and
cellular mechanisms to defend against microbial infiltration. Among the
armamentarium used by the small intestine to defend against microbial
invasion are antimicrobial peptides called defensins. We previously
have shown that gut barrier function is impaired following hemorrhagic
shock, resulting in translocation of bacteria or endotoxin. Using a rat
model, we examined the effect of hemorrhagic shock on
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Induction of a Rat Enteric Defensin Gene by
Hemorrhagic Shock
-defensin
expression. We utilized the anchored reverse transcriptase PCR strategy
to isolate a rat enteric defensin cDNA. The cDNA is 406 bases in length
and encodes a putative prepro-enteric defensin that we have named rat
defensin 5 (RD-5). RD-5 expression is restricted to the small intestine
and is specifically localized by in situ hybridization to the Paneth
cells. A 10-fold increase in its steady state levels was observed in
the distal intestine immediately after the termination of shock. This
is the first study to show that enteric defensins are inducible
following injury. We suggest that enteric defensins may contribute to
the complex and integrated barrier function of the intestinal mucosal surface.
*
Corresponding author. Mailing address: Department of
Surgery, University of Medicine and Dentistry of New Jersey, MSB-G516 South Orange Ave., Newark, NJ 07103. Phone: (973) 972-1258. Fax: (973)
972-6803. E-mail: condonmr{at}umdnj.edu.
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