A infecção pelo Helicobacter pylori cagA positivo apresenta maior expressão de A IL-8 e CCR-2

Abstract

Introduction: Helicobacter pylori (H. pylori ) is an important etiologic agent of several diseases of the upper digestive tract such as gastritis, peptic ulcer and gastric cancer. The expression of virulence factors by the bacterium, especially the cagA gene contributes to a greater pathogenicity of the bacterium in the gastric mucosa. Objectives: to study the gastric antrum mucosa of patients infected with H. pylori and to compare with the clinical history, clinical and surgical history, concomitant diseases, data from the examination of upper digestive endoscopy, anatomopathological examination and analyze the expression of virulence factors cagA , sites of phosphorylation CagA EPIYA, vacA , iceA1, iceA2 e babA 2, and its influence on the expression of TLR-4 , IL-8 , CCL-2 and CCR-2 in individuals with active gastrites and H. pylori positive. Material and Methods: Were evaluated 126 patients submitted to the examination of upper digestive endoscopy (UDE) with clinical complaints of the upper digestive tract. For this evaluation, before the UDE examination, a clinical questionnaire was made and during the endoscopic examination, multiple biopsies of the esophagus, gastric body and antrum and rapid urease test were performed. The material obtained was sent to the pathology laboratory for anatomopathological examination (APE) and part of the material from the gastric antrum was identified the positivity of H. pylori through the expression of the 16S rRNA gene. Of these, 38 (30.1%) patients presented H. pylori positive, distributed as follows: 32 (84.2%) with active gastritis and 6 (15.8%) without active gastritis. It has been researched these samples with positive H. pylori the expression of cagA, the phosphorylation sites CagA EPIYA, vacAm1, vacAm2, vacAs, vacAs2, iceA1, iceA2, bab2, TLR-4, IL-8, CCL-2 and CCR-2, by PCR. Results: We did not find any clinical data that could be related to the presence of H. pylori infection in the stomach. Endoscopic findings that have relevance to the presence of bacteria was gastritis in both antrum and in the gastric corpus (p <0.05). Patients who used Proton Pump Inhibitors (PPI) showed a decrease in the positivity of the bacteria in the antrum and in the gastric body (p<0.05). The presence of gastritis in the gastric body or gastric antrum had significance with the positivity of the bacterium (p<0.05). In active gastric antrum gastritis, in 20 (95.2%) samples the cagA gene was expressed; the genotype CagA EPIYA ABC was the most frequent and positive in 11 (28.9%) samples; 12 (31.6%) the vacAm1; 16 (42.1%) the vacAm2; 16 (42.1%) the vacAs1 and 12 (31.6%) the vacAs2; 11(28.9%) iceA1 and 17 (44.7%) iceA2 and the babA2 gene in 4 (10.5%). There is a significant prevalence of these factors in the active form of the disease. IL-8 expression was higher in cagA positive individuals; while CCR-2 expression was higher in H. pylori positive individuals. Conclusions: H. pylori infection showed no clinical factor predictive of their presence. In the UDE, the presence of gastritis in the antrum was highlighted as a probable infection of the bacterium. The use of PPIs should be discontinued for at least two weeks prior to UDE to avoid false negatives of the presence of H. pylori in the stomach. The APE was necessary to classify the different gastritis and/or histopathological alterations caused by the bacterium. The study of the presence of the cagA gene and the CagA EPIYA phosphorylation sites are important, but it is still short of routine exams in daily practice. Individuals positive H. pylori and positive cagA present higher IL-8 and CCR- 2 expression in the antral mucosa, thus suggesting that these molecules may be associated with exacerbation of the immune response and aggravation of lesions in the gastric antrum.: