Effect of Helicobacter pylori Eradication on TLR2 and TLR4 Expression in Patients with Gastric Lesions

Autor(es)

Targa Cadamuro, Aline Cristina ; Teixeira Rossi, Ana Flavia ; Biselli-Perico, Joice Matos ; Pereira, Patricia Fucuta ; Bedin Mascarin Do Vale, Edla Polsinelli ; Acayaba, Ricardo ; Moreira Leite, Ktia Ramos ; Goloni-Bertollo, Eny Maria ; Silva, Ana Elizabete

• Tipo de documento: Artigo Científico
• Fonte: Mediators of Inflammation; v. 2015, p. 9-pg., 2015-01-01.

Resumo

Objective. Helicobacter pylori (Hp) is recognized by TLR4 and TLR2 receptors, which trigger the activation of genes involved in the host immune response. Thus, we evaluated the effect of eradication therapy on TLR2 and TLR4 mRNA and protein expression in H. pylori-infected chronic gastritis patients (CG-Hp+) and 3 months after treatment. Methods. A total of 37 patients CG-Hp+ were evaluated. The relative quantification (RQ) of mRNA was assessed by TaqMan assay and protein expression by immunohistochemistry. Results. Before treatment both TLR2 and TLR4 mRNA in CG-Hp+ patients were slightly increased (TLR2 = 1.32; TLR4 = 1.26) in relation to Hp-negative normal gastric mucosa (P <= 0.05). After successful eradication therapy no significant change was observed (TLR2 = 1.47; TLR4 = 1.53; P > 0.05). In addition, the cagA and vacA bacterial genotypes did not influence the gene expression levels, and we observed a positive correlation between the RQ values of TLR2 and TLR4, both before and after treatment. Immunoexpression of the TLR2 and TLR4 proteins confirmed the gene expression results. Conclusion. In conclusion, the expression of both TLR2 and TLR4 is increased in CG-Hp+ patients regardless of cagA and vacA status and this expression pattern is not significantly changed after eradication of bacteria, at least for the short period of time evaluated. (AU)

• Processo FAPESP: 12/15036-8 - Avaliação da expressão gênica e protéica em processos inflamatórios e neoplasias do trato digestório: estômago e colorretal
• Beneficiário: Ana Elizabete Silva
• Modalidade de apoio: Auxílio à Pesquisa - Regular