Enteric infection with Citrobacter rodentium induces coagulative liver necrosis and hepatic inflammation prior to peak infection and colonic disease

Acute and chronic forms of inflammation are known to affect liver responses and susceptibility to disease and injury. Furthermore, intestinal microbiota has been shown critical in mediating inflammatory host responses in various animal models. Using C. rodentium, a known enteric bacterial pathogen,...

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Published in:PloS one 2012-03, Vol.7 (3), p.e33099-e33099
Main Authors: Raczynski, Arkadiusz R, Muthupalani, Sureshkumar, Schlieper, Katherine, Fox, James G, Tannenbaum, Steven R, Schauer, David B
Format: Article
Language:English
Subjects:
Analysis
Analysis of Variance
Animal models
Animals
Bacteria
Bioengineering
Biology
Cellular signal transduction
Chemokines - blood
Chronic infection
Citrobacter
Citrobacter rodentium
Colon
Colonic Diseases - microbiology
Colonization
Cytochrome
Cytokines
Cytokines - blood
Defects
Disease
Diseases
E coli
Edema
Engineering
Enzymes
Escherichia coli
Gangrene
Gastrointestinal diseases
Hepatitis
Hepatitis - microbiology
Homeostasis
House mouse
Immunoblotting
Immunohistochemistry
Infections
Inflammation
Inflammatory bowel disease
Injuries
Intestinal microflora
Intestine
Ischemia
Liver
Liver - microbiology
Liver - pathology
Medicine
Metabolism
Mice
Mice, Inbred C57BL
Microbiota
Microbiota (Symbiotic organisms)
Necrosis
Necrosis - microbiology
Pathogenesis
Pathogens
Proteins
Rodents
Signal transduction
Signal Transduction - physiology
Statistics, Nonparametric
Stress
transaminase
Transaminases
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creator Raczynski, Arkadiusz R
Muthupalani, Sureshkumar
Schlieper, Katherine
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Tannenbaum, Steven R
Schauer, David B
description Acute and chronic forms of inflammation are known to affect liver responses and susceptibility to disease and injury. Furthermore, intestinal microbiota has been shown critical in mediating inflammatory host responses in various animal models. Using C. rodentium, a known enteric bacterial pathogen, we examined liver responses to gastrointestinal infection at various stages of disease pathogenesis. For the first time, to our knowledge, we show distinct liver pathology associated with enteric infection with C. rodentium in C57BL/6 mice, characterized by increased inflammation and hepatitis index scores as well as prominent periportal hepatocellular coagulative necrosis indicative of thrombotic ischemic injury in a subset of animals during the early course of C. rodentium pathogenesis. Histologic changes in the liver correlated with serum elevation of liver transaminases, systemic and liver resident cytokines, as well as signal transduction changes prior to peak bacterial colonization and colonic disease. C. rodentium infection in C57BL/6 mice provides a potentially useful model to study acute liver injury and inflammatory stress under conditions of gastrointestinal infection analogous to enteropathogenic E. coli infection in humans.
doi_str_mv 10.1371/journal.pone.0033099
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identifier ISSN: 1932-6203
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1932-6203
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source Open Access: PubMed Central; Publicly Available Content Database
subjects Analysis
Analysis of Variance
Animal models
Animals
Bacteria
Bioengineering
Biology
Cellular signal transduction
Chemokines - blood
Chronic infection
Citrobacter
Citrobacter rodentium
Colon
Colonic Diseases - microbiology
Colonization
Cytochrome
Cytokines
Cytokines - blood
Defects
Disease
Diseases
E coli
Edema
Engineering
Enzymes
Escherichia coli
Gangrene
Gastrointestinal diseases
Hepatitis
Hepatitis - microbiology
Homeostasis
House mouse
Immunoblotting
Immunohistochemistry
Infections
Inflammation
Inflammatory bowel disease
Injuries
Intestinal microflora
Intestine
Ischemia
Liver
Liver - microbiology
Liver - pathology
Medicine
Metabolism
Mice
Mice, Inbred C57BL
Microbiota
Microbiota (Symbiotic organisms)
Necrosis
Necrosis - microbiology
Pathogenesis
Pathogens
Proteins
Rodents
Signal transduction
Signal Transduction - physiology
Statistics, Nonparametric
Stress
transaminase
Transaminases
title Enteric infection with Citrobacter rodentium induces coagulative liver necrosis and hepatic inflammation prior to peak infection and colonic disease
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