Lack of association among TNF-alfa gene expression, -308 polymorphism (G > A) and virulence markers of Helicobacter pylori
J. venom. anim. toxins incl. trop. dis
; J. venom. anim. toxins incl. trop. dis;21: 1-7, 31/03/2015. tab
Article
em En
| LILACS, VETINDEX
| ID: biblio-1484647
Biblioteca responsável:
BR68.1
Localização: BR68.1
ABSTRACT
Background Tumor necrosis factor plays a critical role in the pathogenesis of gastric diseases such as gastric cancer, and an abnormal inflammatory response has frequently been observed in dyspeptic patients. Helicobacter pylori infection can induce a gastric mucosal inflammatory response that may be influenced by -308 (G > A) polymorphisms and gene expression of theTNF- gene. Methods One hundred and thirty-four gastric biopsy samples were collected from patients of both genders (61 and 73, mean age 40.3 ± 24.2 years) with gastric symptoms. The -308 (G > A) polymorphism of TNF- was characterized using polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). The expression level was measured using real-time PCR, and relative quantification (RQ) was calculated using the comparative CT method (2-CT). Results The analysis revealed an increase in TNF- gene expression in patients with gastritis; on the other hand, no statistical differences were observed in patients with gastric cancer. In addition, no association was found among -308 polymorphism genotypes, virulence markers, or TNF- gene expression. Conclusions Helicobacter pylori induces a large increase in TNF- expression in patients with gastritis, regardless of tissue inflammation, but after the tissue becomes neoplastic, the presence of bacteria did not influence expression. These results suggest that the TNF- pathway may play an important role in the progression from gastritis to gastric cancer.
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Texto completo:
1
Coleções:
01-internacional
Base de dados:
LILACS
/
VETINDEX
Assunto principal:
Polimorfismo Genético
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Neoplasias Gástricas
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Helicobacter pylori
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Fator de Necrose Tumoral alfa
Tipo de estudo:
Risk_factors_studies
Limite:
Animals
Idioma:
En
Revista:
J. venom. anim. toxins incl. trop. dis
Ano de publicação:
2015
Tipo de documento:
Article
/
Project document