Helicobacter bilis Infection Accelerates and H. hepaticus Infection Delays the Development of Colitis in Multiple Drug Resistance-Deficient (mdr1a−/−) Mice
| Autor: | Phil Morrissey, Donna Shows, Kim Waggie, Sabine S. Escobar, Lillian Maggio-Price, Weiping Zeng, Andrew Burich, Joanne L. Viney |
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| Rok vydání: | 2002 |
| Předmět: |
Helicobacter bilis
ATP Binding Cassette Transporter Subfamily B Immunoglobulins Mice Transgenic Inflammatory bowel disease Helicobacter Infections Pathology and Forensic Medicine Mice Helicobacter medicine Animals Mesenteric lymph nodes Lymphocytes Colitis biology Body Weight Animal Models Inflammatory Bowel Diseases medicine.disease biology.organism_classification Ulcerative colitis Drug Resistance Multiple Intestines medicine.anatomical_structure Immunology Cytokines ATP-Binding Cassette Transporters Female Helicobacter hepaticus Crypt Abscess |
| Zdroj: | The American Journal of Pathology. 160:739-751 |
| ISSN: | 0002-9440 |
| Popis: | mdr1a-deficient mice lack P-glycoprotein and spontaneously develop colitis with age. Helicobacter spp. are gram-negative organisms that have been associated with colitis in certain mouse strains, but Helicobacter spp. have been excluded as contributing to the spontaneous colitis that develops in mdr1a-/- mice. We wished to determine whether infection with either H. bilis or H. hepaticus would accelerate the development of inflammatory bowel disease (IBD) in mdr1a-/- mice. We found that H. bilis infection induced diarrhea, weight loss, and IBD in mdr1a-/- mice within 6 to 17 weeks post-inoculation and before the expected onset of spontaneous IBD. Histopathology of H. bilis-induced IBD included crypt hyperplasia, inflammatory cell infiltrates, crypt abscesses, and obliteration of normal gut architecture. Reverse transcription-polymerase chain reaction and Taqman analysis from colonic tissue showed increased transcripts for interferon-gamma and interleukin-10 from H. bilis-infected colitic mdr1a-/- mice. Additionally, mesenteric lymph nodes had increased cellularity with expansion of CD4+ and CD8+ T cells and B cells and increased proliferation to soluble H. bilis antigens with elaboration of interferon-gamma, tumor necrosis factor-alpha and interleukin-10. In contrast, H. hepaticus infection of mdr1a-/- mice did not accelerate disease but rather delayed the onset of spontaneous colitis which was milder in severity. mdr1a-/- mice infected with Helicobacter spp. may provide a useful tool to explore the pathogenesis of microbial-induced IBD in a model with a presumed epithelial cell "barrier" defect. |
| Databáze: | OpenAIRE |
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