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  4. Enteric Infection with Citrobacter rodentium Induces Coagulative Liver Necrosis and Hepatic Inflammation Prior to Peak Infection and Colonic Disease

Enteric Infection with Citrobacter rodentium Induces Coagulative Liver Necrosis and Hepatic Inflammation Prior to Peak Infection and Colonic Disease

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Author(s)
Raczynski, Arkadiusz R.
•
Muthupalani, Sureshkumar
•
Schlieper, Katherine Ann
•
Fox, James G.
•
Tannenbaum, Steven Robert
•
Schauer, David B.
Date Issued
March 2012
Journal
PLoS ONE
Publisher
Public Library of Science
Citation
Raczynski, Arkadiusz R. et al. “Enteric Infection with Citrobacter Rodentium Induces Coagulative Liver Necrosis and Hepatic Inflammation Prior to Peak Infection and Colonic Disease.” Ed. Bernhard Ryffel. PLoS ONE 7.3 (2012): e33099. Web.
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Final published version
Abstract
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.
MIT Department
Massachusetts Institute of Technology. Department of Biological Engineering
Massachusetts Institute of Technology. Division of Comparative Medicine
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Creative Commons Attribution
http://creativecommons.org/licenses/by/2.5/
Persistent DSpace Link
http://hdl.handle.net/1721.1/70940
DOI of Published Version
https://doi.org/10.1371/journal.pone.0033099
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