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1 Department of Pediatrics and Steele Memorial Children's Research Center, University of Arizona, Tucson, AZ, USA
2 Department of Microbiology and Immunology, University of Arizona, Tucson, AZ, USA
3 Department of Cell Biology and Anatomy, University of Arizona, Tucson, AZ, USA
4 Department of Pediatrics and Steele Memorial Children's Research Center, University of Arizona, Tucson, AZ, USA; Department of Cell Biology and Anatomy, University of Arizona, Tucson, AZ, USA
* To whom correspondence should be addressed. E-mail: mhalpern{at}peds.arizona.edu.
Necrotizing enterocolitis (NEC) is a common and devastating gastrointestinal disease of premature infants. Along with pathologic effects in the ileum, severe NEC is often accompanied by multisystem organ failure, including liver failure. The aim of this study was to determine the potential changes in hepatic cytokines and inflammatory mediators during experimental NEC. The well-established neonatal rat model of NEC was used in this study, and changes in liver morphology, numbers of Kupffer cells (KC), gene expression and histologic localization of IL-18, TNF
, and inducible nitric oxide synthase (NOS2) were evaluated. Intestinal luminal TNF levels also were measured. Production of hepatic IL-18 and TNF and numbers of KC were increased in rats with NEC compared to controls and correlated with the progression of intestinal damage during NEC development. Further, increased levels of TNF in the intestinal lumen of rats with NEC was significantly decreased when KC were inhibited with gadolinium chloride. These results suggest an important role of the liver and the gut/liver axis in the pathogenesis of NEC.
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