An eighteen-month helicobacter infection does not induce amyloid plaques or neuroinflammation in brains of wild type C57BL/6J mice

Claire Roubaud Baudron, Lucie Chambonnier, Alice Buissionnière, Alban Giese, Nathalie Macrez, Yoon Cho, Valérie Fénelon, Lucie Blaszczyk, Pierre Dubus, Philippe Lehours, Francis Mégraud, Nathalie Salles, Christine Varon
JAD. 2015-04-13; 45(4): 1045-1050
DOI: 10.3233/JAD-143129

Lire sur PubMed

Baudron CR, Chambonnier L, Buissionnière A, Giese A, Macrez N, Cho Y, Fénelon V, Blaszczyk L, Dubus P, Lehours P, Mégraud F, Salles N, Varon C.

There is increasing evidence to support the role of infectious agents in the progression of Alzheimer’s disease (AD), especially Helicobacter pylori (H. pylori). The impact of Helicobacter infection on the brain of non-AD predisposed mice was studied. For that, C57BL/6J mice were infected by oral gavage with H. pylori SS1 (n = 6) and Helicobacter felis (H. felis) (n=6) or not infected (n = 6) for evaluation of neuroinflammation (anti-GFAP and anti-iba1 immunohistochemistry) and amyloid-β deposition (thioflavin-S stain and anti-Aβ  immunohistochemistry). After 18-month of infection, H. pylori SS1 and H. felis infection induced a strong gastric inflammation compared to non-infected mice, but did not induce brain neuroinflammation or amyloid-β deposition.


Auteurs Bordeaux Neurocampus