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Article

Helicobacter pylori Urease: Potential Contributions to Alzheimer’s Disease

1
Laboratory of Neurotoxins, Brain Institute of Rio Grande do Sul (BRAINS) and Graduate Program in Medicine and Health Sciences, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre CEP 90610-000, RS, Brazil
2
Center of Biotechnology, Graduate Program in Cellular and Molecular Biology, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre CEP 91501-970, RS, Brazil
3
Laboratory of Cognition and Memory Neurobiology, Brain Institute of Rio Grande do Sul (BRAINS) and Graduate Program in Biomedical Gerontology, Pontifical Catholic University of Rio Grande do Sul (PUCRS), Porto Alegre CEP 90610-000, RS, Brazil
*
Author to whom correspondence should be addressed.
These authors have contributed equally to this work.
Academic Editors: Alexander Tonevitsky and Diana Maltseva
Int. J. Mol. Sci. 2022, 23(6), 3091; https://doi.org/10.3390/ijms23063091
Received: 18 December 2021 / Revised: 9 March 2022 / Accepted: 10 March 2022 / Published: 13 March 2022
Alzheimer’s disease (AD) causes dementia and memory loss in the elderly. Deposits of beta-amyloid peptide and hyperphosphorylated tau protein are present in a brain with AD. A filtrate of Helicobacter pylori’s culture was previously found to induce hyperphosphorylation of tau in vivo, suggesting that bacterial exotoxins could permeate the blood–brain barrier and directly induce tau’s phosphorylation. H. pylori, which infects ~60% of the world population and causes gastritis and gastric cancer, produces a pro-inflammatory urease (HPU). Here, the neurotoxic potential of HPU was investigated in cultured cells and in rats. SH-SY5Y neuroblastoma cells exposed to HPU (50–300 nM) produced reactive oxygen species (ROS) and had an increased [Ca2+]i. HPU-treated BV-2 microglial cells produced ROS, cytokines IL-1β and TNF-α, and showed reduced viability. Rats received daily i.p., HPU (5 µg) for 7 days. Hyperphosphorylation of tau at Ser199, Thr205 and Ser396 sites, with no alterations in total tau or GSK-3β levels, and overexpression of Iba1, a marker of microglial activation, were seen in hippocampal homogenates. HPU was not detected in the brain homogenates. Behavioral tests were performed to assess cognitive impairments. Our findings support previous data suggesting an association between infection by H. pylori and tauopathies such as AD, possibly mediated by its urease. View Full-Text
Keywords: Helicobacter pylori; urease; neuroinflammation; tau hyperphosphorylation; pro-inflammatory cytokines; object recognition test; elevated plus maze; SH-SY5Y neuroblastoma cells; BV-2 microglia Helicobacter pylori; urease; neuroinflammation; tau hyperphosphorylation; pro-inflammatory cytokines; object recognition test; elevated plus maze; SH-SY5Y neuroblastoma cells; BV-2 microglia
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MDPI and ACS Style

Uberti, A.F.; Callai-Silva, N.; Grahl, M.V.C.; Piovesan, A.R.; Nachtigall, E.G.; Furini, C.R.G.; Carlini, C.R. Helicobacter pylori Urease: Potential Contributions to Alzheimer’s Disease. Int. J. Mol. Sci. 2022, 23, 3091. https://doi.org/10.3390/ijms23063091

AMA Style

Uberti AF, Callai-Silva N, Grahl MVC, Piovesan AR, Nachtigall EG, Furini CRG, Carlini CR. Helicobacter pylori Urease: Potential Contributions to Alzheimer’s Disease. International Journal of Molecular Sciences. 2022; 23(6):3091. https://doi.org/10.3390/ijms23063091

Chicago/Turabian Style

Uberti, Augusto F., Natalia Callai-Silva, Matheus V. C. Grahl, Angela R. Piovesan, Eduarda G. Nachtigall, Cristiane R. G. Furini, and Celia Regina Carlini. 2022. "Helicobacter pylori Urease: Potential Contributions to Alzheimer’s Disease" International Journal of Molecular Sciences 23, no. 6: 3091. https://doi.org/10.3390/ijms23063091

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