Reversibility of heterotopic proliferative glands in glandular stomach of Helicobacter pylori-infected Mongolian gerbils on eradication.
Helicobacter pylori (Hp) infection is an important factor in human gastric disorders. Mongolian gerbils can be easily infected with Hp and represent excellent experimental models to clarify the role of Hp in chronic active gastritis, peptic ulcers, intestinal metaplasia, and gastric carcinoma. We have proved the enhancing effects of Hp infection on all histological types of gastric cancers in Mongolian gerbils exposed to chemical carcinogens. Heterotopic proliferative glands (HPGs) also frequently develop with Hp infection in the glandular stomach of infected gerbils, with a slightly dysplastic change of constituent cells. Distinguishing reversible inflammatory lesions from true neoplasms upon eradication is necessary for further biological or histochemical investigations using this model. We employed an experimental model of long-term Hp infection and eradication in gerbils. HPGs finally developed with a phenotypic shift of intestinalization with Paneth cells. After eradication, HPGs were obviously reduced, and gastric lesions in mucosa also improved with few remnants of the former injury. This shows that reversible HPGs are frequently induced solely by Hp infection in this animal species, and are related to severe gastritis, rather than being malignant in character. Thus, distinguishing reversible lesions from true neoplasms is necessary to investigate the relationship of Hp infection and gastric carcinogenesis in this animal model.
Nozaki
Koji
K
Division of Oncological Pathology, Aichi Cancer Center Research Institute, Chikusa-ku, Nagoya, Aichi 464-8681, Japan.
Shimizu
Nobuyuki
N
Tsukamoto
Tetsuya
T
Inada
Ken-Ichi
K
Cao
Xueyuan
X
Ikehara
Yuzuru
Y
Kaminishi
Michio
M
Sugiyama
Atsushi
A
Tatematsu
Masae
M
D000818:Animals; D049109:Cell Proliferation; D003094:Collagen / Q000378:metabolism; D004195:Disease Models, Animal; D005753:Gastric Mucosa / Q000382:microbiology* / Q000473:pathology; D005756:Gastritis / Q000473:pathology; D005849:Gerbillinae / Q000382:microbiology*; D016481:Helicobacter Infections / Q000473:pathology*; D016480:Helicobacter pylori / Q000378:metabolism*; D008679:Metaplasia / Q000473:pathology; D009077:Mucins / Q000378:metabolism; D010641:Phenotype; D013270:Stomach / Q000382:microbiology* / Q000473:pathology; D013997:Time Factors; D014456:Ulcer / Q000473:pathology
D009077:Mucins; D003094:Collagen