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Fig. 7 | Inflammation and Regeneration

Fig. 7

From: Helicobacter pylori infection in the stomach induces neuroinflammation: the potential roles of bacterial outer membrane vesicles in an animal model of Alzheimer’s disease

Fig. 7

A working hypothesis on the roles of HP-OMVs in Alzheimer’s disease (AD) pathology. HP colonizes in the stomach chronically and produces OMVs that disrupt tight junctions in the gut epithelium. Through the “leaky” gut, HP-OMVs may enter the bloodstream. Next, the circulating HP-OMVs can increase the permeability of the blood-brain barrier (BBB), resulting in BBB breakdown which allows HP-OMVs to enter the brain parenchyma. In the brain, OMVs cause activation and/or migration of microglia and astrocytes as well as enhance neuronal damage initiated by amyloid-β or tau, accelerating neuronal loss. This would lead to neuroinflammation adjacent to increased amyloid plaques, contributing to AD pathology. Events possibly caused by HP are in red

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Inflammation and Regeneration

ISSN: 1880-8190

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