Abstract
Infection of the gastric mucosa by Helicobacter spp. is an important cause of gastric diseases and neoplasms in humans and animals. The objective of this study was to evaluate the presence of Helicobacter spp. in the livers of dogs with nonspecific histological changes. The association between Helicobacter spp. infection, hepatocyte proliferation and E-cadherin expression was also evaluated. Liver samples from 39 dogs were subjected to polymerase chain reaction (PCR) to identify Helicobacter spp. Hepatocyte proliferation was evaluated by the AgNOR method. The Helicobacter genus was detected in seven (17.9%) animals that exhibited liver histological changes. Twenty-six animals were PCR negative and exhibited microscopical changes, while six animals demonstrated no histological changes and were PCR negative. Infected animals showed a significant increase in liver lesional score and the area of NORs compared to non-infected dogs. E-cadherin expression showed no significant difference among groups. The results suggest that Helicobacter spp. and hepatocytes injury in the livers of dogs could contribute to increased cell proliferation, thereby influencing hepatocarcinogenesis. Key words: Dog, helicobacter, liver, AgNOR, immunohistochemistry, E-cadherin.
Highlights
Helicobacter infection is considered an important cause of stomach disease and gastric neoplasia in humans (Buckley and O’Morain, 1998; Morgner et al, 2000)
Samples considered normal were negative by polymerase chain reaction (PCR) (n = 6), and they were used as the control group (G1)
The association between Helicobacter species DNA in liver and liver diseases such as cirrhosis and hepatocellular carcinoma has led to the hypothesis that these bacteria may play a role in the evolution of hepatic lesions (Rocha et al, 2005)
Summary
Helicobacter infection is considered an important cause of stomach disease and gastric neoplasia in humans (Buckley and O’Morain, 1998; Morgner et al, 2000). Helicobacter pylori is the main species that infects humans; its pathogenicity is attributed to factors that induce cell proliferation and apoptosis such as production of adhesins and cytotoxins (Blaser and Atherton, 2004; Galmiche et al, 2000). Infection can cause disruption of the gastric mucosal barrier and induce the release of inflammatory mediators that enhance apoptosis and cell turnover (Peek et al, 2010).
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