Document Detail


Role of IL-10 in hepatocyte tight junction alteration in mouse model of experimental colitis.
MedLine Citation:
PMID:  12393933     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: A variety of hepatobiliary abnormalities have been described in patients with chronic inflammatory bowel diseases (IBDs). The purpose of this study was to investigate the role of endogenous IL-10 in alteration of hepatocyte TJ paracellular barrier and in the rapid transcytotic vesicular pathway modification associated with intestinal inflammation. MATERIALS AND METHODS: To address this question, we used an experimental model of colitis, induced by dinitrobenzene sulfonic acid (DNBS). When compared to DNBS-treated IL-10 wild-type (IL-10WT) mice, DNBS-treated IL-10 knock-out mice (IL-10KO) mice experienced a higher rate of the extent and severity of the histological signs of colon injury. RESULTS: Colon and liver levels of the pro-inflammatory cytokines tumour necrosis factor, interleukin-1 beta and interleukin-6 were also greatly enhanced in IL-10KO mice in comparison to wild-type mice. Liver histology from IL-10KO and IL-10WT did not show any parenchymal and portal tract inflammation at 4 days after DNBS administration. Serum total bilirubin and Alanine aminotransferase, were significantly increased in DNBS-IL-10KO mice vs. DNBS-IL-10KO mice. Therefore, we found an increase of tight junctional permeability to lanthanum nitrate (molecular weight, 433) in the livers from DNBS-treated IL-10WT mice; lanthanum accumulated throughout the junctional area up to the most apical region bordering the lumen. Absence of a functional IL-10 gene in IL-10KO mice resulted in a significant augmentation of apical diffusion of lanthanum after DNBS-induced colitis. Immunofluorescent labelling of frozen liver sections from DNBS-IL10KO mice, immunolocalization for and claudin-1 and ZO-1 resulted in a significant alteration in the localization of the immunosignals for claudin-1 and ZO-1 after DNBS administration in comparison with DNBS-IL10WT. CONCLUSION: In conclusion, we suggest that the absence of IL-10 may represent an important pathophysiological mechanism of hepatobiliary injuries and cholestasis observed in patients with IBD.
Authors:
Emanuela Mazzon; Domenico Puzzolo; Achille P Caputi; Salvatore Cuzzocrea
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Publication Detail:
Type:  Comparative Study; Journal Article    
Journal Detail:
Title:  Molecular medicine (Cambridge, Mass.)     Volume:  8     ISSN:  1076-1551     ISO Abbreviation:  Mol. Med.     Publication Date:  2002 Jul 
Date Detail:
Created Date:  2002-10-23     Completed Date:  2003-04-16     Revised Date:  2008-11-20    
Medline Journal Info:
Nlm Unique ID:  9501023     Medline TA:  Mol Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  353-66     Citation Subset:  IM    
Affiliation:
Department of Biomorphology, School of Medicine, Messina, Italy.
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MeSH Terms
Descriptor/Qualifier:
Alanine Transaminase / blood,  drug effects
Animals
Benzenesulfonates
Bilirubin / blood
Colitis / chemically induced,  pathology*,  physiopathology
Colon / drug effects,  pathology,  physiopathology
Cytokines / analysis
Disease Models, Animal*
Hepatocytes / drug effects,  pathology*,  ultrastructure
Interleukin-10 / physiology*
Lanthanum / pharmacokinetics
Liver / drug effects,  pathology,  physiopathology
Mice
Mice, Inbred C57BL
Mice, Knockout
Tight Junctions / drug effects,  pathology*,  ultrastructure
Chemical
Reg. No./Substance:
0/Benzenesulfonates; 0/Cytokines; 12379-41-8/dinitrobenzenesulfonic acid; 130068-27-8/Interleukin-10; 635-65-4/Bilirubin; 7439-91-0/Lanthanum; EC 2.6.1.2/Alanine Transaminase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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