A distinctive set of genes is upregulated during the inflammation-carcinoma sequence in mouse stomach infected by Helicobacter felis.
J Histochem Cytochem
; 55(3): 263-74, 2007 Mar.
Article
in En
| MEDLINE
| ID: mdl-17101721
ABSTRACT
Helicobacter pylori infects over half the population worldwide and is a leading cause of chronic gastritis and gastric cancer. However, the mechanism by which this organism induces inflammation and carcinogenesis is not fully understood. In the present study we used insulin-gastrin (INS-GAS) transgenic mice that fully develop gastric adenocarcinoma after infection of H. pylori-related Helicobacter felis. Histological examination revealed that more than half of those mice developed invasive adenocarcinoma after 8 months of infection. These carcinomas were stained by NCC-ST-439 and HECA-452 that recognize 6-sulfated and non-sulfated sialyl Lewis X. Lymphocytic infiltration predominantly to submucosa was observed in most H. felis-infected mice, and this was associated with the formation of peripheral lymph node addressin (PNAd) on high endothelial venule (HEV)-like vessels detected by MECA-79. Time-course analysis of gene expression by using gene microarray revealed upregulation of several inflammation-associated genes including chemokines, adhesion molecules, surfactant protein D (SP-D), and CD74 in the infected stomach. Immunohistochemical analysis demonstrated that SP-D is expressed in hyperplasia and adenocarcinoma whereas CD74 is expressed in adenocarcinoma in situ and invasive carcinoma. These results as a whole indicate that H. felis induces HEV-like vessels and inflammation-associated chemokines and chemokine receptors, followed by adenocarcinoma formation.
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Collection:
01-internacional
Database:
MEDLINE
Main subject:
Stomach Neoplasms
/
Adenocarcinoma
/
Helicobacter Infections
/
Gene Expression Profiling
/
Helicobacter felis
/
Gastric Mucosa
/
Gastritis
Limits:
Animals
Language:
En
Journal:
J Histochem Cytochem
Journal subject:
HISTOCITOQUIMICA
Year:
2007
Document type:
Article
Affiliation country:
United States