Are Mucosa CD4+/CD8+ T-cells Expressions Correlated with the Endoscopic Appearance of Chronic Gastritis Related with H.pylori Infection?

摘要

Background. Local inflammatory processes in the gastric mucosa are followed by extensive immune cell infiltration resulting in chronic active gastritis characterized by a marked infiltration of T(h)1 cytokine-producing CD4+ and CD8+T-cells.Objective. To investigate the correlation between CD4+/CD8+ T-cells in gastric mucosa with endoscopic appearance in chronic gastritis with or without H.pylori infection.Methods. This prospective cross sectional study was performed in a chronic dyspepsia population in July-November 2009 at the Dr. Sardjito General Hospital Yogyakarta, Indonesia. The update Sydney system was used to analyze the gastroscopy appearance. Biopsy specimens were stained with HE-stain and IHC-stain. Data were analyzed by t-test, Mann-Whitney and Spearman correlation test.Results. 88 consecutive subjects were enrolled in the study (50% male; 50% female), age 46±15 years; 25% H.pylori positive. The expression of CD4+ and CD8+ were higher in H.pylori negative subjects, but only the CD4+ was significant (p= 0.011). A significant correlation was found between CD4+ and CD8+ in both subjects (r(Hp+) = 0.62 and r(Hp-)= 0.68; p<0.05). The expression of CD4+ and CD8+ in H.pylori positive showed a significant correlation with gastric lesions (r(CD4+)= -0.60; r(CD8+)= -0.42 ; p<0.05), only erosion showed a significant difference in both subjects.Conclusion. A positive correlation was found between CD4+ and CD8+ infiltration in both subjects with or without H.pylori infection, and a negative correlation was only found between gastric lesion with CD4+ and CD8+ infiltration in H.pylori subject. Introduction Dyspepsia is the most common problem encountered in gastroenterology practice. Multiple and diverse causes influence structural disorders, treatment, degree of inflammation and metabolic disorders.1Helicobacter pylori (H.pylori) is the most important cause of chronic active gastritis, gastro-duodenal ulcers and plays an important role in the development of gastric cancer and mucosa-associated lymphatic tissue (MALT) lymphomas. Helicobacter pylori colonizes in approximately 50% of the world’s population, resulting in persistent stomach inflammation in infected individuals.1,2 In Asia, the prevalence of H.pylori infection varies markedly in different Asian countries. Higher prevalence rates are found in developing Asian countries while lower rates have been reported in more industrialized and developed countries.3 Prevalence of H.pylori infection at Yogyakarta, Indonesia, based on positive IgG H.pylori, is lower than Japanese people (5% vs. 62% in men and 4% vs. 57% women).4Persistent gastro-duodenal infection causes the H.pylori to produce humoral and cellular immune response.5,6,7 Mucosal inflammation in acute H.pylori infection is a response of humoral immune (involves IgM) caused by invasive H.pylori or water-soluble proteins passing the mucosal barrier. Acute infection of H.pylori may induce mucosal infiltration dominated by neutrophils, and within a few weeks develops into chronic active inflammations dominated by neutrophils, macrophages, lymphocytes, and plasma cells. High expressions of CD4+ T-cells gastric mucosa are usually present in H.pylori acute infections as a dominant role of regulating or suppressing local inflammation. CD8+ T-cells take a role in initiating and maintaining gastric inflammation. Both CD4+ and CD8+ T-cells are present in chronic active H.pylori infection.8,9,10There are few studies that are concerned in investigating the correlation between objective parameters such as endoscopic features and pathological examinations. To further explore the correlation between CD4+and CD8+ T-cell infiltration in gastric mucosa with endoscopic features in patients with chronic dyspepsia H.pylori infection, a clinical investigation was designed with an analytical method as proposed in this study. Material and Method PatientsA total of 88 consecutive adult patients with chronic gastritis who were diagnosed through g