Helicobacter pylori（H.pylori） infection is a recognized risk factor of dementia, while its role and mechanism in Alzheimer disease（AD） remained unclarified. Our previous study has identified that injection of solu...Helicobacter pylori（H.pylori） infection is a recognized risk factor of dementia, while its role and mechanism in Alzheimer disease（AD） remained unclarified. Our previous study has identified that injection of soluble H.pylori filtrate could induce AD-like pathologic changes and cognitive impairment in SD rats. In the present study, we further explored the effect of long-term stomach colonization of H.pylori bacteria on the brains of SD rats. The results showed that H.pylori bacteria gavage induced an efficient colonization of H.pylori in the stomach after four weeks. However, there was no significant change of tau phosphorylation at Thr205（pT205）, Thr231（pT231）, Ser396（pS396） and Ser404（pS404） sites in the hippocampus and cerebral cortex. The H.pylori-infected rats also showed no cognitive impairment. These observations may result from inefficient release of bacterial pathogenic factors or the overall lack of host inflammatory responses. We conclude that SD rat with long-term H.pylori colonization in the stomach is not a suitable animal model for exploring the effects of H.pylori infection on brain function in human beings; administration of bacterial filtrates may better reveal the systemic pathologic changes induced by bacterial infection in animals which show a negative host response to bacterial colonization.展开更多
基金supported by the research foundation from Hubei Health and Family Planning Commission(No.WJ2015MB152)Natural Science Foundation of Hubei Province,China(No.2015CKC897 and No.2017CFA065)+1 种基金National Natural Science Foundation of China(No.81471304 and No.31771189)Integrated Innovative Team for Major Human Diseases Program of Tongji Medical College,HUST
文摘Helicobacter pylori（H.pylori） infection is a recognized risk factor of dementia, while its role and mechanism in Alzheimer disease（AD） remained unclarified. Our previous study has identified that injection of soluble H.pylori filtrate could induce AD-like pathologic changes and cognitive impairment in SD rats. In the present study, we further explored the effect of long-term stomach colonization of H.pylori bacteria on the brains of SD rats. The results showed that H.pylori bacteria gavage induced an efficient colonization of H.pylori in the stomach after four weeks. However, there was no significant change of tau phosphorylation at Thr205（pT205）, Thr231（pT231）, Ser396（pS396） and Ser404（pS404） sites in the hippocampus and cerebral cortex. The H.pylori-infected rats also showed no cognitive impairment. These observations may result from inefficient release of bacterial pathogenic factors or the overall lack of host inflammatory responses. We conclude that SD rat with long-term H.pylori colonization in the stomach is not a suitable animal model for exploring the effects of H.pylori infection on brain function in human beings; administration of bacterial filtrates may better reveal the systemic pathologic changes induced by bacterial infection in animals which show a negative host response to bacterial colonization.
