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Inflammation Is Attenuated In Germ‐free C57BL/6 Mice Infected with Helicobacter felis
Author(s) -
Schmitz Julia M,
Schoeb Trenton R,
McCracken Vance J,
Lorenz Robin G
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.852.8
Subject(s) - specific pathogen free , biology , helicobacter , bacteria , stomach , felis , cancer , microbiology and biotechnology , inflammation , helicobacter pylori , temperature gradient gel electrophoresis , pathogen , gastric mucosa , stomach cancer , immunology , 16s ribosomal rna , medicine , cats , genetics , biochemistry , virus
Specific pathogen free (SPF) C57BL/6 mice infected with Helicobacter felis develop gastric cancer after 12 – 15 months. Unpublished studies using denaturing gradient gel electrophoresis (DGGE) indicated the presence of additional bacterial types in H. felis infected mice relative to mock mice. We hypothesize that changes that occur in the stomach during progression to gastric cancer, including increased pH and changes in the mucous layer, allow other bacteria to colonize the stomach and perhaps contribute to cancer progression. To test whether such bacteria could affect the progression to cancer, germ free (GF) B6 and SPF B6 mice were mock infected or infected with H. felis for sixteen weeks. Stomachs were analyzed by RT‐PCR and ELISAs for cytokine expression, DGGE for analysis of bacterial populations, and immunohistochemistry for histological analysis. A trend toward decreased inflammation (mean score of 6.3 on a scale of 0–9) and epithelial tissue destruction was observed in infected GF.B6 mice compared to SPF B6 mice (mean score of 9). To further evaluate the additive effect of other bacteria on the progression to gastric cancer, SPF and GF B6 mice will be infected for a year. The function of the additional bacteria in the SPF B6 mice remains to be elucidated but could be evaluated by adding specific bacteria identified by DGGE analysis. [NIH T32 AI07041, R01 DK59911 and ACS]