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   <subfield code="a">10.1007/s10620-011-1701-3</subfield>
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   <subfield code="a">Helicobacter bilis Colonization Enhances Susceptibility to Typhlocolitis Following an Inflammatory Trigger</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Zhiping Liu, Amanda Ramer-Tait, Abigail Henderson, Cumhur Demirkale, Dan Nettleton, Chong Wang, Jesse Hostetter, Albert Jergens, Michael Wannemuehler]</subfield>
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   <subfield code="a">Background: Aberrant mucosal immune responses to antigens of the resident microbiota are a significant cause of inflammatory bowel diseases (IBD), as are genetic and environmental factors. Previous work from our laboratory demonstrated that Helicobacter bilis colonization of immunocompetent, defined microbiota mice induced antigen-specific immune responses to the resident microbiota, yet these mice failed to develop colitis, suggesting that the immunological provocation induced by H. bilis alone was insufficient to induce disease. Aim: The purpose of this study was to test the hypothesis that the introduction of a bacterial provocateur such as H. bilis enhances the host's susceptibility to IBD following an inflammatory event. Methods: Defined microbiota (DM) mice colonized with H. bilis were administered low dose (1.5%) dextran sodium sulfate (DSS) in drinking water for 5days followed by a 4-day restitution period. Severity of lesions was assessed grossly and microscopically. Differential expression of select mucosal genes and histopathologic lesions was characterized. Results: Helicobacter bilis colonization increased the severity of intestinal inflammation induced by an inflammatory trigger in the form of low-dose DSS. An analysis of the molecular and cellular mechanisms associated with H. bilis colonization revealed significant increases in expression of mucosal genes associated with lymphocyte activation and inflammatory cell chemotaxis as well as increased infiltration of mucosal macrophages and T cells in mice colonized with H. bilis prior to DSS treatment versus DSS treatment alone. Conclusions: These results indicate that prior colonization with H. bilis heightens the host's sensitivity to enteric inflammation by altering mucosal homeostasis and initiating immune cell activation and migration.</subfield>
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   <subfield code="a">Springer Science+Business Media, LLC, 2011</subfield>
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   <subfield code="a">Helicobacter bilis</subfield>
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   <subfield code="a">Immune cells</subfield>
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   <subfield code="a">Chemotaxis</subfield>
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   <subfield code="a">Activation</subfield>
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   <subfield code="a">Liu</subfield>
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   <subfield code="u">Department of Veterinary Microbiology and Preventive Medicine, College of Veterinary Medicine, Iowa State University, Room 2182, 50011-1250, Ames, IA, USA</subfield>
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   <subfield code="u">Department of Veterinary Microbiology and Preventive Medicine, College of Veterinary Medicine, Iowa State University, Room 2182, 50011-1250, Ames, IA, USA</subfield>
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   <subfield code="a">Henderson</subfield>
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   <subfield code="u">Department of Veterinary Microbiology and Preventive Medicine, College of Veterinary Medicine, Iowa State University, Room 2182, 50011-1250, Ames, IA, USA</subfield>
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   <subfield code="u">Department of Statistics, College of Liberal Arts and Sciences, Iowa State University, Ames, IA, USA</subfield>
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   <subfield code="a">Wang</subfield>
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   <subfield code="u">Department of Veterinary Microbiology and Preventive Medicine, College of Veterinary Medicine, Iowa State University, Room 2182, 50011-1250, Ames, IA, USA</subfield>
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