title: Progressive proliferative and dysplastic typhlocolitis in aging syrian hamsters naturally infected with Helicobacter spp.: a spontaneous model of inflammatory bowel disease.
abstract: Helicobacter spp. have been implicated in a variety of gastrointestinal tract diseases, including peptic ulcer disease, gastric cancer, and inflammatory bowel disease (IBD), in humans and animals. Although most models of IBD are experimentally induced, spontaneous or natural models of IBD are rare. Herein, we describe a long-term study of chronic, progressive lesions that develop in the distal portion of the large bowel of unmanipulated Syrian hamsters naturally infected with Helicobacter spp. Twenty-four Syrian hamsters of three age groups (group A, 1 month [n = 4], group B, 7-12 months [n = 12], group C, 18-24 months [n = 12]), underwent complete postmortem examination. Results of microbial isolation and polymerase chain reaction and restriction fragment length polymorphism analyses confirmed the presence of Helicobacter spp. infection in the distal portion of the large bowel of all animals. Additionally, confounding pathogens, such as Clostridium difficile, Lawsonia intracellularis, and Giardia spp. that can cause proliferative enteritis, were absent in the hamsters of this study. Histopathologic scores for inflammation (P < 0.01), hyperplasia (P < 0.01), and dysplasia (P < 0.05) were significantly higher in the ileocecocolic (ICC) junction of animals in group C, relative to group A. Dysplastic lesions of various grades were detected in 5 of 11 hamsters in group C. Interestingly, the segment of the bowel that is usually colonized by Helicobacter spp. in hamsters had the most severe lesions. One hamster of group C developed a malignant fibrous histiocytoma, whereas another hamster developed a round cell sarcoma originating from the ICC junction. Thus, lesions in the distal portion of the large bowel of aging hamsters naturally colonized with Helicobacter spp. warrants developing the hamster as an animal model of IBD and potentially IBD-related cancer.
authors.affiliation: Prashant R Nambiar, Division of Comparative Medicine, Massachusetts Institute of Technology, Building 16-849, Cambridge, MA 02139, USA. nambiar@mit.edu
authors.forename: P R
authors.initials: PR
authors.lastname: Nambiar
authors.forename: S M
authors.initials: SM
authors.lastname: Kirchain
authors.forename: K
authors.initials: K
authors.lastname: Courmier
authors.forename: S
authors.initials: S
authors.lastname: Xu
authors.forename: N S
authors.initials: NS
authors.lastname: Taylor
authors.forename: E J
authors.initials: EJ
authors.lastname: Theve
authors.forename: M M
authors.initials: MM
authors.lastname: Patterson
authors.forename: J G
authors.initials: JG
authors.lastname: Fox
mesh_terms: D000818:Animals; D006224:Cricetinae; D003601:Cytotoxicity Tests, Immunologic; D004195:Disease Models, Animal; D020345:Enterocolitis, Necrotizing / Q000382:microbiology / Q000473:pathology*; D006367:HeLa Cells; D016998:Helicobacter / Q000235:genetics*; D016481:Helicobacter Infections / Q000473:pathology*; D006801:Humans; D007150:Immunohistochemistry; D015212:Inflammatory Bowel Diseases / Q000382:microbiology / Q000473:pathology*; D007420:Intestine, Large / Q000382:microbiology / Q000473:pathology; D008647:Mesocricetus; D012150:Polymorphism, Restriction Fragment Length