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Interleukin 10 reduces lethality and hepatic injury induced by lipopolysaccharide in galactosamine-sensitized mice.

Abstract：

BACKGROUND & AIMS:Tumor necrosis factor alpha (TNF-alpha) release plays a pivotal role in the pathogenesis of liver injury induced by lipopolysaccharide (LPS) administration in D-galactosamine (GalN)-sensitized mice. Interleukin (IL) 10 is an anti-inflammatory cytokine that inhibits TNF-alpha synthesis and release both in vitro and in vivo and prevents lethality from experimental endotoxemia. The present study was designed to ascertain whether in vivo treatment with IL-10 protects mice against LPS/GalN-induced liver injury. METHODS:Mice were treated with an intraperitoneal dose of LPS/GalN with or without IL-10 pretreatment. Liver injury was assessed biochemically and histologically, and plasma TNF-alpha levels, liver myeloperoxidase activity, and adhesion molecule expression were determined. RESULTS:Administration of LPS in GalN-sensitized mice caused lethal shock and massive hepatic necrosis in almost 100% of the mice. The effect was associated with a significant increase in plasma TNF-alpha concentrations, liver myeloperoxidase activity, and up-regulation of adhesion molecules on liver specimens and circulating neutrophils. Pretreatment with IL-10 reduced plasma TNF-alpha concentrations and LPS/GalN-induced liver injury and lethality. Moreover, IL-10 reduced the LPS/GalN-induced liver neutrophil margination and up-regulation of adhesion molecules both on liver specimens and circulating neutrophils. CONCLUSIONS:The present results suggest that IL-10 therapy could be useful in the treatment of TNF-alpha-mediated liver diseases.

journal_name

Gastroenterology

journal_title

Gastroenterology

authors

Santucci L,Fiorucci S,Chiorean M,Brunori PM,Di Matteo FM,Sidoni A,Migliorati G,Morelli A

doi

10.1053/gast.1996.v111.pm8780580

subject

Has Abstract

pub_date

1996-09-01 00:00:00

pages

736-44

issue

3

eissn

0016-5085

issn

1528-0012

pii

S0016508596004076

journal_volume

111

pub_type

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