Hofer, Sandra; Grandgirard, Denis; Burri, Denise; Fröhlich, Tanja K.; Leib, Stephen L. (2011). Bacterial meningitis impairs hippocampal neurogenesis. Journal of neuropathology and experimental neurology, 70(10), pp. 890-899. Hagerstown, Md.: Lippincott Williams & Wilkins 10.1097/NEN.0b013e3182303f31
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Bacterial meningitis causes persisting neurofunctional sequelae. Theoccurrence of apoptotic cell death in the hippocampal subgranular zone of the dentate gyrus characterizes the disease in patients and relates to deficits in learning and memory in corresponding experimental models. Here, we investigated why neurogenesis fails to regenerate the damage in the hippocampus associated with the persistence of neurofunctional deficits. In an infant rat model of bacterial meningitis, the capacity of hippocampal-derived cells to multiply and form neurospheres was significantly impaired comparedto that in uninfected littermates. In an in vitro model of differentiating hippocampal cells, challenges characteristic of bacterial meningitis (i.e. bacterial components, tumor necrosis factor [20 ng/mL], or growth factor deprivation) caused significantly more apoptosis in stem/progenitor cells and immature neurons than in mature neurons. These results demonstrate that bacterial meningitis injures hippocampal stem and progenitor cells, a finding that may explain the persistence of neurofunctional deficits after bacterial meningitis.
Item Type: |
Journal Article (Original Article) |
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Division/Institute: |
04 Faculty of Medicine > Service Sector > Institute for Infectious Diseases 04 Faculty of Medicine > Service Sector > Institute for Infectious Diseases > Research |
UniBE Contributor: |
Hofer, Sandra, Grandgirard, Denis, Leib, Stephen |
ISSN: |
0022-3069 |
Publisher: |
Lippincott Williams & Wilkins |
Language: |
English |
Submitter: |
Factscience Import |
Date Deposited: |
04 Oct 2013 14:24 |
Last Modified: |
05 Dec 2022 14:07 |
Publisher DOI: |
10.1097/NEN.0b013e3182303f31 |
PubMed ID: |
21937913 |
Web of Science ID: |
000295117900005 |
BORIS DOI: |
10.7892/boris.8284 |
URI: |
https://boris.unibe.ch/id/eprint/8284 (FactScience: 213801) |