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Male Syrian Hamsters Experimentally Infected with H elicobacter spp. of the H . bilis Cluster Develop MALT ‐Associated Gastrointestinal Lymphomas
Author(s) -
Woods Stephanie E.,
Ek Courtney,
Shen Zeli,
Feng Yan,
Ge Zhongming,
Muthupalani Sureshkumar,
Whary Mark T.,
Fox James G.
Publication year - 2016
Publication title -
helicobacter
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 79
eISSN - 1523-5378
pISSN - 1083-4389
DOI - 10.1111/hel.12265
Subject(s) - hamster , lymphoma , feces , biology , malt lymphoma , gastrointestinal tract , pathology , helicobacter , gastroenterology , microbiology and biotechnology , immunology , medicine , helicobacter pylori , biochemistry , genetics
Background Aged hamsters naturally infected with novel H elicobacter spp. classified in the H . bilis cluster develop hepatobiliary lesions and typhlocolitis. Methods To determine whether enterohepatic H . spp. contribute to disease, H elicobacter ‐free hamsters were experimentally infected with H . spp. after suppression of intestinal bacteria by tetracycline treatment of dams and pups. After antibiotic withdrawal, weanlings were gavaged with four H . bilis ‐like H elicobacter spp. isolated from hamsters or H . bilis ATCC 43879 isolated from human feces and compared to controls (n = 7 per group). Results Helicobacter bilis 43879‐dosed hamsters were necropsied at 33 weeks postinfection ( WPI ) due to the lack of detectable infection by fecal PCR ; at necropsy, 5 of 7 were weakly PCR positive but lacked intestinal lesions. The remaining hamsters were maintained for ~95 WPI ; chronic H . spp. infection in hamsters (6/7) was confirmed by PCR , bacterial culture, fluorescent in situ hybridization, and ELISA . Hamsters had mild‐to‐moderate typhlitis, and three of the male H . spp.‐infected hamsters developed small intestinal lymphoma, in contrast to one control. Of the three lymphomas in H . spp.‐infected hamsters, one was a focal ileal mucosa‐associated lymphoid tissue ( MALT ) B ‐cell lymphoma, while the other two were multicentric small intestinal large B ‐cell lymphomas involving both the MALT and extra‐ MALT mucosal sites with lymphoepithelial lesions. The lymphoma in the control hamster was a diffuse small intestinal lymphoma with a mixed population of T and B cells. Conclusions Results suggest persistent H . spp. infection may augment risk for gastrointestinal MALT origin lymphomas. This model is consistent with H . pylori/heilmannii ‐associated MALT lymphoma in humans and could be further utilized to investigate the mechanisms of intestinal lymphoma development.