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Am J Physiol Gastrointest Liver Physiol 284: G695-G702, 2003. First published January 15, 2003; doi:10.1152/ajpgi.00353.2002
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Vol. 284, Issue 4, G695-G702, April 2003

Hepatic inflammatory mediators contribute to intestinal damage in necrotizing enterocolitis

Melissa D. Halpern1, Hana Holubec2, Jessica A. Dominguez1, Yolanda G. Meza1, Catherine S. Williams1, Miriam C. Ruth1, Robert S. McCuskey3, and Bohuslav Dvorak1,3

1 Department of Pediatrics and Steele Memorial Children's Research Center, 2 Department of Microbiology and Immunology, and 3 Department of Cell Biology and Anatomy, University of Arizona, Tucson, Arizona 85724

Necrotizing enterocolitis (NEC) is a common and devastating gastrointestinal disease of premature infants. Along with pathological effects in the ileum, severe NEC is often accompanied by mutisystem organ failure, including liver failure. The aim of this study was to determine the changes in hepatic cytokines and inflammatory mediators in 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 histological localization of IL-18, TNF-alpha , and inducible nitric oxide synthase were evaluated. Intestinal luminal TNF-alpha levels were also measured. Production of hepatic IL-18 and TNF-alpha and numbers of KC were increased in rats with NEC and correlated with the progression of intestinal damage during NEC development. Furthermore, increased levels of TNF-alpha 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 NEC pathogenesis.

gastrointestinal system; inflammation; neonatal; gut-liver axis


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