Objective:The distribution and correlation between Helicobacter pylori(Hp)infection and non-atrophic gastritis,gastric ulcer,intraepithelial neoplasm and gastric cancer were investigated by statistical methods,and the clinical significance was discussed.Furthermore,the expression changes of Treg and Th17 cells in gastric mucosal tissue biopsy of patients with Hp infection-related atrophic gastritis accompanied by enterification were further analyzed,and the significance of the changes of Treg/Th17 immune balance in Hp infection-related atrophic gastritis accompanied by enterification was discussed.In order to make some exploration of immunotherapy for Hp infection-related stomach diseases,especially for precancerous lesions such as atrophic gastritis with intestinal metaplasia.Methods:Part 1:In this study,2081 patients from Third People’s Hospital of Hubei Province Affiliated to Jianghan University during 2019-2021 were selected.C13 breath test,serological antibody test,gastroscopy and pathological examination were performed.According to the diagnosis of gastroscopy and pathology,the patients were divided into 5groups:917 patients with non-atrophic gastritis,636 patients with atrophic gastritis,406patients with gastric ulcer,89 patients with intraepithelial neoplasia and 33 patients with gastric cancer.The correlation between different virulence types of Hp infection and the age of patients and gastroscopic pathological types was analyzed statistically.Part II:Immunohistochemical staining was performed on tissues with obvious lesions and normal gastric mucosa in Hp infected atrophic gastritis with intestinal metaplasia and non-atrophic gastritis,to investigate the levels and expressions of Foxp3 and IL-17 cells in Hp infected atrophic gastritis with intestinal metaplasia.Results:Part I:There were 2081 patients,including 1034 males and 1047 females.Serological antibody test results showed that 977 were Hp-positive and 1104 were Hp-negative.By comparing the age of patients with different types of Hp infection and gastric mucosal lesions,the mean age of non-atrophic gastritis in Hp typeⅠgroup,Hp typeⅡgroup and Hp-negative group was lower than that in atrophic gastritis,gastric ulcer,intraepithelial neoplasia and gastric cancer groups,the difference was statistically significant(p<0.05).The mean age of non-atrophic gastritis and atrophic gastritis patients in Hp groupⅠwas significantly lower than that in Hp groupⅡand Hp negative group,and the differences were statistically significant(p<0.05).There were no significant differences in the mean age of patients with gastric ulcer,intraepithelial neoplasia and gastric cancer among the three groups(p>0.05).The Hp infection rate of each group from high to low was gastric cancer group,intraepithelial neoplasia group,atrophic gastritis group,gastric ulcer group and non-atrophic gastritis group,and the difference was statistically significant(p<0.05).The positive rate of Hp typeⅠwas higher than that of Hp typeⅡ,and the difference was statistically significant(p<0.05).There was statistical significance in comparing the positive rate of Hp typeⅠand Hp typeⅡin each group(p<0.05).Cytotoxin-associated protein A(Cag A),vacuolar toxin A(Vac A)and urease(Ure)were compared among all groups,and the differences were statistically significant(p<0.05).In 653 Hp positive patients,Cag A+Vac A antibody(60.0%)was the main type,higher than Cag A antibody(36.7%)and Vac A antibody(3.2%),the difference was statistically significant(p<0.05).Among the 324patients with positive Hp type II,the positive rate of Ure B antibody(64.8%)in each group was higher than that of Ure A+Ure B antibody(30.5%)and Ure A antibody(4.6%)in this group,and the difference was statistically significant(p<0.05).Part II:The expression levels of Foxp3 and IL-17 cells in Hp infected atrophic gastritis with intestinal metaplasia were higher than those in normal non-atrophic gastritis in gastric mucosa,with statistical significance(p<0.05).Conclusions:1.Different types of Hp infection can show different pathogenicity in gastric mucosal lesions,especially type I Hp infection can accelerate the course of gastric diseases.2.Hp infection can promote gastric mucosa atrophy,and it is possible to reverse or slow down gastric mucosa atrophy if Hp is completely removed within a certain period of time.3.Foxp3 and IL-17 cells are up-regulated in Hp infected atrophic gastritis with intestinal metaplasia,suggesting that Foxp3and IL-17 may accelerate the progression of gastric mucosa atrophy.4.It is further speculated that Treg and Th17 cells may accumulate in the early tumor microenvironment in the stage of precancerous lesions such as Hp infection with atrophic gastritis and intestinal metaplasia. |