Long-term Helicobacter pylori Infection Does Not Induce Tauopathy and Memory Impairment in SD Rats

• Published in: Current medical science Vol. 37; no. 6; pp. 823 - 827
• Main Author: 周欢;郭英;李行;刘杨震宇;申屠杨萍;景小鹏;梁珈玮;周新文;王小川;王建枝;曾吉;刘蓉
• Format: Journal Article
• Language: English
• Published: Wuhan Huazhong University of Science and Technology 01.12.2017; Department of Pathophysiology,Key Laboratory of Ministry of Education for Neurological Disorders,School of Basic Medicine,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430030,China%Department of Clinic Laboratory,Pu Ai Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430033,China%Department of Pathophysiology,Key Laboratory of Ministry of Education for Neurological Disorders,School of Basic Medicine,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430030,China; The Institute for Brain Research,Collaborative Innovation Center for Brain Science,Huazhong University of Science and Technology,Wuhan 430030,China
• Subjects: Medicine; Medicine & Public Health; tau phosphorylation; Alzheimer disease; cognitive impairment; Helicobacter pylori
• ISSN: 1672-0733; 2096-5230; 1993-1352; 1993-1352; 2523-899X
• DOI: 10.1007/s11596-017-1813-x

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.