Helicobacter pylori Makes a Molecular Incision to Gain Epithelial Entry

Noto, Jennifer M.; Peek, Richard M.

doi:10.1016/j.chom.2017.09.014

Cited by 4 publications

(1 citation statement)

References 10 publications

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“…Secretion of serin protease HtrA leads to the cleavage of occludin and claudin-8 (tight junctions) and E-cadherin (adherens junction). Furthermore, virulence factor CagA (cytotoxin-associated gene A) acts on apical-junctional complexes, activates β-catenin and, in its phosphorylated form, can induce cell scattering and morphological changes (reviewed by [ 174 ]). In addition, H. pylori OMVs have been found to carry CagA and to strongly associate with tight junctions, adding another route of modulation [ 175 ].…”

Section: Human Microbiome Dysbiosis As a Source Of A Systemic Chromentioning

confidence: 99%

Complex Interaction between Resident Microbiota and Misfolded Proteins: Role in Neuroinflammation and Neurodegeneration

González-Sanmiguel

Schuh

Muñoz-Montesino

et al. 2020

Cells

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Neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD) and Creutzfeldt–Jakob disease (CJD) are brain conditions affecting millions of people worldwide. These diseases are associated with the presence of amyloid-β (Aβ), alpha synuclein (α-Syn) and prion protein (PrP) depositions in the brain, respectively, which lead to synaptic disconnection and subsequent progressive neuronal death. Although considerable progress has been made in elucidating the pathogenesis of these diseases, the specific mechanisms of their origins remain largely unknown. A body of research suggests a potential association between host microbiota, neuroinflammation and dementia, either directly due to bacterial brain invasion because of barrier leakage and production of toxins and inflammation, or indirectly by modulating the immune response. In the present review, we focus on the emerging topics of neuroinflammation and the association between components of the human microbiota and the deposition of Aβ, α-Syn and PrP in the brain. Special focus is given to gut and oral bacteria and biofilms and to the potential mechanisms associating microbiome dysbiosis and toxin production with neurodegeneration. The roles of neuroinflammation, protein misfolding and cellular mediators in membrane damage and increased permeability are also discussed.

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Section: Human Microbiome Dysbiosis As a Source Of A Systemic Chromentioning

confidence: 99%