Arginase-1 e perfil treg parecem modular processo inflamatório em pacientes com gastrite crônica e IL-33 pode ser a citocina de alarme nos pacientes H.pylori positivo

Abstract

INTRODUCTION: Helicobacter pylori (H. pylori) is a highly prevalent bacterium in our midst and is directly involved in several diseases of the upper digestive tract such as gastritis, peptic ulcer and gastric cancer. In this study, predictive data from the clinical, endoscopic, anatomopathological and immune response mechanisms were investigated against the presence of this bacterium. Immune activating molecules have been described and studied in an attempt to contain H pylori infection. OBJECTIVES: to study the presence of H. pylori infection in the gastric mucosa with the clinical history, medical history, concomitant diseases, and data from the upper digestive endoscopy (UDE) examination of the anatomopathological examination (APE). At imune response, analyse fragments of the gastric body by qPCR, mRNA expression of IFNcytokines, IL-17, IL-10, TGF  , IL-6, IL-22, IL-23, IL-33; of the transcription factors T-bet , ROR  t and FOXP3 ; of the enzymes ARG1, ARG2 and NOS2 ; of the neuropeptides VIP and TAC, and their respective receptors VIPR1, and TAC-R1 . To compare the expression of these genes with the presence or absence of H. pylori bacteria . MATERIAL AND METHODS: were evaluated 126 patients with symptoms of the upper digestive tract and with a clinical indication of Digestive High Endoscopy (UDE) . Before the endoscopy examination a detailed clinical questionnaire was perforemed and during the examination was performed multiple biopsies of the esophagus, gastric body and antrum and rapid urease test. Fragments of the mucosa of the body and the gastric antrum were collected for anatomopathological examination and for analysis of the expression of enzymes, cytokines and transcription factors by real-time PCR , qPCR . RESULTS: no clinical data were found 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 (PPIs) showed a decrease in the positivity of the bacteria in the antrum and in the gastric body (p<0.05) through the APE. The presence of gastritis in the gastric body or gastric antrum was significant with the positivity of the bacterium (p<0,05). The expression of the ARG1 gene was significantly higher in the group of patients with chronic gastritis with no activity when compared to the control group (Kruskal Wallis; p = 0.02). The gene expression of TGF  gene and its transcription factor FOXP3 were significantly higher in the group of chronic no-active gastrites pacientes when compared to the control group. When comparing the expression of IFN  IL-17, IL-10 and TGF  genes and the T-bet and ROR   transcription factors , with the presence or absence of H. pylori , there was no significant difference . However, FOXP3 expression was significantly lower in H. pylori positive patients when compared to H. pylori negative patients (Mann-Whitney, p=0.01). 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. PAD was necessary to classify the differet types of gastritis and/or histopathological changes caused by the bacteria . ARG-1 and Treg profile appear to be modulating the inflammatory process, protecting these patients from tissue lesions with chronic gastritis without activity . Furthermore, we suggest that IL-33 may be a crucial mediator of the immune response to infection after gastric mucosal damage.