CagA
Helicobacter pylori
Opisthorchis viverrini
Cholangiocarcinoma
histopathological study
risk factor
the animal model
Journal
Helicobacter
ISSN: 1523-5378
Titre abrégé: Helicobacter
Pays: England
ID NLM: 9605411
Informations de publication
Date de publication:
Aug 2021
Aug 2021
Historique:
revised:
10
04
2021
received:
24
02
2021
accepted:
05
05
2021
pubmed:
26
5
2021
medline:
1
10
2021
entrez:
25
5
2021
Statut:
ppublish
Résumé
Helicobacter pylori (HP) has been detected in the hepatobiliary tract of cholangiocarcinoma (CCA) patients in regions both endemic and non-endemic for Opisthorchis viverrini (OV) infection. However, whether H. pylori infection promotes CCA development remains unknown. We investigated CCA development in hamsters induced by a combination of infection with H. pylori and administration of N-nitrosodimethylamine (NDMA) and compared findings with those in an OV plus NDMA group. Eighty-five hamsters were divided into four groups: (1) normal, (2) administered NDMA, (3) infected with cagA At 3 months post-infection (p.i.), cholangitis and lymphoid follicles without tumor appearance were noted in the HN group, whereas extensive fibrosis was seen in members of the ON group, 10% of which had developed tumors. At 6 months p.i., 10% of hamsters administered NDMA alone had developed CCA, whereas in the HN and ON groups, 20% and 60% of hamsters, respectively, had developed CCA. Cytokeratin-19 (CK19) expression was observed in the CCA tissues of both the HN and the ON groups, confirming the bile duct origin of the CCA cells. CCA development in the HN group might be inflammation-mediated, as suggested by overexpression of HMGB1, PCNA, IL-8, and 8-OxodG in CCA tissues. cagA
Sections du résumé
BACKGROUND
BACKGROUND
Helicobacter pylori (HP) has been detected in the hepatobiliary tract of cholangiocarcinoma (CCA) patients in regions both endemic and non-endemic for Opisthorchis viverrini (OV) infection. However, whether H. pylori infection promotes CCA development remains unknown. We investigated CCA development in hamsters induced by a combination of infection with H. pylori and administration of N-nitrosodimethylamine (NDMA) and compared findings with those in an OV plus NDMA group.
MATERIALS AND METHODS
METHODS
Eighty-five hamsters were divided into four groups: (1) normal, (2) administered NDMA, (3) infected with cagA
RESULTS
RESULTS
At 3 months post-infection (p.i.), cholangitis and lymphoid follicles without tumor appearance were noted in the HN group, whereas extensive fibrosis was seen in members of the ON group, 10% of which had developed tumors. At 6 months p.i., 10% of hamsters administered NDMA alone had developed CCA, whereas in the HN and ON groups, 20% and 60% of hamsters, respectively, had developed CCA. Cytokeratin-19 (CK19) expression was observed in the CCA tissues of both the HN and the ON groups, confirming the bile duct origin of the CCA cells. CCA development in the HN group might be inflammation-mediated, as suggested by overexpression of HMGB1, PCNA, IL-8, and 8-OxodG in CCA tissues.
CONCLUSION
CONCLUSIONS
cagA
Substances chimiques
Dimethylnitrosamine
M43H21IO8R
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e12817Subventions
Organisme : Thailand Research Fund
ID : MRG6080284
Organisme : Khon Kaen University Research Fund
ID : KKU600095
Organisme : Cholangiocarcinoma Research Institute
ID : 04/2560
Commentaires et corrections
Type : CommentIn
Informations de copyright
© 2021 John Wiley & Sons Ltd.
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