Chlamydia pneumoniae can infect the central nervous system via the olfactory and trigeminal nerves and contributes to Alzheimer's disease risk.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
17 02 2022
Historique:
received: 20 10 2021
accepted: 07 02 2022
entrez: 18 2 2022
pubmed: 19 2 2022
medline: 11 3 2022
Statut: epublish

Résumé

Chlamydia pneumoniae is a respiratory tract pathogen but can also infect the central nervous system (CNS). Recently, the link between C. pneumoniae CNS infection and late-onset dementia has become increasingly evident. In mice, CNS infection has been shown to occur weeks to months after intranasal inoculation. By isolating live C. pneumoniae from tissues and using immunohistochemistry, we show that C. pneumoniae can infect the olfactory and trigeminal nerves, olfactory bulb and brain within 72 h in mice. C. pneumoniae infection also resulted in dysregulation of key pathways involved in Alzheimer's disease pathogenesis at 7 and 28 days after inoculation. Interestingly, amyloid beta accumulations were also detected adjacent to the C. pneumoniae inclusions in the olfactory system. Furthermore, injury to the nasal epithelium resulted in increased peripheral nerve and olfactory bulb infection, but did not alter general CNS infection. In vitro, C. pneumoniae was able to infect peripheral nerve and CNS glia. In summary, the nerves extending between the nasal cavity and the brain constitute invasion paths by which C. pneumoniae can rapidly invade the CNS likely by surviving in glia and leading to Aβ deposition.

Identifiants

pubmed: 35177758
doi: 10.1038/s41598-022-06749-9
pii: 10.1038/s41598-022-06749-9
pmc: PMC8854390
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2759

Informations de copyright

© 2022. The Author(s).

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Auteurs

Anu Chacko (A)

Menzies Health Institute Queensland, Griffith University, Gold Coast campus, Southport, QLD, Australia.

Ali Delbaz (A)

Menzies Health Institute Queensland, Griffith University, Gold Coast campus, Southport, QLD, Australia.

Heidi Walkden (H)

Menzies Health Institute Queensland, Griffith University, Gold Coast campus, Southport, QLD, Australia.

Souptik Basu (S)

Menzies Health Institute Queensland, Griffith University, Gold Coast campus, Southport, QLD, Australia.

Charles W Armitage (CW)

School of Immunology and Microbial Sciences, King's College London, London, UK.

Tanja Eindorf (T)

Menzies Health Institute Queensland, Griffith University, Gold Coast campus, Southport, QLD, Australia.

Logan K Trim (LK)

Centre for Immunology and Infection Control, School of Biomedical Sciences, Queensland University of Technology, Brisbane, Australia.

Edith Miller (E)

Menzies Health Institute Queensland, Griffith University, Gold Coast campus, Southport, QLD, Australia.

Nicholas P West (NP)

Menzies Health Institute Queensland, Griffith University, Gold Coast campus, Southport, QLD, Australia.

James A St John (JA)

Menzies Health Institute Queensland, Griffith University, Gold Coast campus, Southport, QLD, Australia.
Griffith Institute for Drug Discovery, Griffith University, Nathan campus, Brisbane Queensland, Australia.

Kenneth W Beagley (KW)

Centre for Immunology and Infection Control, School of Biomedical Sciences, Queensland University of Technology, Brisbane, Australia.

Jenny A K Ekberg (JAK)

Menzies Health Institute Queensland, Griffith University, Gold Coast campus, Southport, QLD, Australia. j.ekberg@griffith.edu.au.
Griffith Institute for Drug Discovery, Griffith University, Nathan campus, Brisbane Queensland, Australia. j.ekberg@griffith.edu.au.

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