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Esophageal Helicobacter pylori colonization aggravates esophageal injury caused by reflux.
- Source :
-
World journal of gastroenterology [World J Gastroenterol] 2014 Nov 14; Vol. 20 (42), pp. 15715-26. - Publication Year :
- 2014
-
Abstract
- Aim: To investigate esophageal Helicobacter pylori (H. pylori) colonization on esophageal injury caused by reflux and the related mechanisms.<br />Methods: An esophagitis model, with acid and bile reflux, was surgically produced in male rats. The rats were randomly divided into either: (1) an esophagogastroduodenal anastomosis (EGDA) group; (2) an EGDA with H. pylori infection group; (3) a pseudo-operation with H. pylori infection group; or (4) a pseudo-operation group. All rats were kept for 36 wk. Based on the location of H. pylori colonization, the EGDA rats with H. pylori infection were subdivided into those with concomitant esophageal H. pylori colonization or those with only gastric H. pylori colonization. The esophageal injuries were evaluated grossly and microscopically. The expressions of CDX2 and MUC2 were determined by real-time polymerase chain reaction (RT-PCR) and immunohistochemistry. Ki-67 antigen expression was determined by immunohistochemistry. The mRNA levels of cyclin D1, c-Myc, Bax and Bcl-2 were determined by RT-PCR. Cell apoptosis was evaluated using the TdT-mediated dUTP nick-end labeling method.<br />Results: Esophagitis, Barrett's esophagus (BE), and esophageal adenocarcinoma (EAC) developed in rats that underwent EGDA. When comparing rats with EGDA and concomitant esophageal H. pylori colonization to EGDA-only rats, the severity of injury (87.9 ± 5.2 vs 77.2 ± 8.6, macroscopically, 92.5 ± 8.0 vs 83.8 ± 5.5, microscopically, both P < 0.05) and the incidences of BE (80.0% vs 33.3%, P = 0.055) and EAC (60.0% vs 11.1%, P < 0.05) were increased. These increases were associated with upregulation of CDX2 and MUC2 mRNA (10.1 ± 5.4 vs 3.0 ± 2.9, 8.4 ± 4.6 vs 2.0 ± 3.2, respectively, Ps < 0.01) and protein (8.1 ± 2.3 vs 3.3 ± 3.1, 7.3 ± 4.0 vs 1.8 ± 2.7, respectively, all P < 0.05). The expression of Ki-67 (8.9 ± 0.7 vs 6.0 ± 1.7, P < 0.01) and the presence of apoptotic cells (8.3 ± 1.1 vs 5.3 ± 1.7, P < 0.01) were also increased significantly in rats with EGDA and concomitant esophageal H. pylori colonization compared with rats with EGDA only. The mRNA levels of cyclin D1 (5.8 ± 1.9 vs 3.4 ± 1.3, P < 0.01), c-Myc (6.4 ± 1.7 vs 3.7 ± 1.2, P < 0.01), and Bax (8.6 ± 1.6 vs 5.1 ± 1.3, P < 0.01) were significantly increased, whereas the mRNA level of Bcl-2 (0.6 ± 0.3 vs 0.8 ± 0.3, P < 0.01) was significantly reduced in rats with EGDA and concomitant esophageal H. pylori colonization compared with rats with EGDA only.<br />Conclusion: Esophageal H. pylori colonization increases esophagitis severity, and facilitates the development of BE and EAC with the augmentation of cell proliferation and apoptosis in esophageal mucosa.
- Subjects :
- Adenocarcinoma genetics
Adenocarcinoma metabolism
Adenocarcinoma pathology
Animals
Apoptosis
Barrett Esophagus genetics
Barrett Esophagus metabolism
Barrett Esophagus pathology
CDX2 Transcription Factor
Cell Proliferation
Cyclin D1 genetics
Cyclin D1 metabolism
Disease Models, Animal
Esophageal Neoplasms genetics
Esophageal Neoplasms metabolism
Esophageal Neoplasms pathology
Esophagitis, Peptic genetics
Esophagitis, Peptic metabolism
Esophagitis, Peptic pathology
Esophagus metabolism
Esophagus pathology
Gene Expression Regulation
Helicobacter Infections complications
Helicobacter Infections genetics
Helicobacter Infections metabolism
Helicobacter Infections pathology
Homeodomain Proteins genetics
Homeodomain Proteins metabolism
Ki-67 Antigen metabolism
Male
Mucin-2 genetics
Mucin-2 metabolism
Proto-Oncogene Proteins c-bcl-2 genetics
Proto-Oncogene Proteins c-bcl-2 metabolism
Proto-Oncogene Proteins c-myc genetics
Proto-Oncogene Proteins c-myc metabolism
RNA, Messenger metabolism
Rats, Sprague-Dawley
Severity of Illness Index
Transcription Factors genetics
Transcription Factors metabolism
bcl-2-Associated X Protein genetics
bcl-2-Associated X Protein metabolism
Adenocarcinoma microbiology
Barrett Esophagus microbiology
Esophageal Neoplasms microbiology
Esophagitis, Peptic microbiology
Esophagus microbiology
Gastroesophageal Reflux complications
Helicobacter Infections microbiology
Helicobacter pylori pathogenicity
Subjects
Details
- Language :
- English
- ISSN :
- 2219-2840
- Volume :
- 20
- Issue :
- 42
- Database :
- MEDLINE
- Journal :
- World journal of gastroenterology
- Publication Type :
- Academic Journal
- Accession number :
- 25400455
- Full Text :
- https://doi.org/10.3748/wjg.v20.i42.15715