Characterization of cecal gene expression in a differentially susceptible mouse model of bacterial-induced inflammatory bowel disease.

Characterization of cecal gene expression in a differentially susceptible mouse model of bacterial-induced inflammatory bowel disease. Research Abstract Details 

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Characterization of cecal gene expression in a differentially susceptible mouse model of bacterial-induced inflammatory bowel disease. Abstract Text:

Matthew H Myles,Brian K Dieckgraefe,Jennifer M Criley,Craig L Franklin,

BACKGROUND: A/JCr mice develop typhlitis in response to Helicobacter hepaticus infection, whereas C57BL/6 mice coexist with this bacterium in a "commensal" relationship and do not develop disease even during prolonged colonization. METHODS: To determine mechanisms that control this balance between responsiveness and nonresponsiveness, the mucosal response of A/JCr and C57BL/6 mice to acute H. hepaticus colonization was evaluated using genome-wide profiling. Transcription levels for a subset of gene discoveries were then evaluated longitudinally by semiquantitative real-time reverse-transcriptase polymerase chain reaction (RT-PCR) to identify changes in gene expression that occur during progression from the acute to chronic phase of colonization. To determine whether chronic mucosal inflammation in A/JCr mice was mediated through a Th1 mechanism, as was inferred from the gene expression data, mice with typhlitis were treated with neutralizing antibody targeting IL-12/23p40 or IFN-gamma and the response to treatment was determined by cecal lesion severity and transcription of disease-related genes. RESULTS: A/JCr mice had a biphasic expression of proinflammatory genes that corresponded with the acute and chronic phases of disease. In contrast, C57BL/6 mice exhibited a less robust acute transcriptional response that waned by day 30 postinoculation. Sustained upregulation of proinflammatory signals and responsiveness to anti-IL-12/23p40 and anti-IFN-gamma antibody suggests that inflammation in A/JCr mice was mediated through a Th1 mechanism. Prolonged upregulation of SOCS3 during the acute response to colonization suggests that C57BL/6 mice maintain mucosal homeostasis, at least in part by attenuating responsiveness to cytokine signaling. CONCLUSIONS: Collectively, these findings provide a foundation for understanding the immunological mechanisms that confer resistance or susceptibility to H. hepaticus-induced typhlitis.

Characterization of cecal gene expression in a differentially susceptible mouse model of bacterial-induced inflammatory bowel disease. Publishing Authors By Initials

MH Myles,BK Dieckgraefe,JM Criley,CL Franklin,

For similar digestive system diseases: gastrointestinal diseases: gastroenteritis: typhlitis research abstracts see: digestive system diseases: gastrointestinal diseases: gastroenteritis: typhlitis research

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Characterization of cecal gene expression in a differentially susceptible mouse model of bacterial-induced inflammatory bowel disease. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Inflammatory bowel diseases

VOLUME: 13

Page Numbers: 822-36

Journal Abbreviation: Inflamm. Bowel Dis.

ISSN: 1078-0998

DAY: 3

MONTH: Jul

YEAR: 2007

Characterization of cecal gene expression in a differentially susceptible mouse model of bacterial-induced inflammatory bowel disease. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 9508162

Characterization of cecal gene expression in a differentially susceptible mouse model of bacterial-induced inflammatory bowel disease. Keywords Mesh Terms:

KEYWORDS: Typhlitis

MESH TERMS: pathology

Chemical & Substance for Abstract: Characterization of cecal gene expression in a differentially susceptible mouse model of bacterial-induced inflammatory bowel disease. Information

Substance Name: Suppressor of Cytokine Signaling Protein

Registry Number: 0

Grant and Affiliation Information for Characterization of cecal gene expression in a differentially susceptible mouse model of bacterial-induced inflammatory bowel disease.

AFFILIATION: Research Animal Diagnostic Laboratory, Department of Veterinary Pathobiology, University of Missouri, Columbia, Missouri 65211, USA. mylesm@missouri.edu

Country: United States

AGENCY: United States NIDDK

GRANT: P30-DK052574-07

ACRONYM: DK

MEDLINETA: Inflamm Bowel Dis

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