KCC1 Activation protects Mice from the Development of Experimental Cerebral Malaria.
- Publisher:
- NATURE PUBLISHING GROUP
- Publication Type:
- Journal Article
- Citation:
- Sci Rep, 2019, 9, (1), pp. 6356
- Issue Date:
- 2019-04-23
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Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author |
Hortle, E |
|
dc.contributor.author | Starrs, L | |
dc.contributor.author | Brown, FC | |
dc.contributor.author | Jane, SM | |
dc.contributor.author | Curtis, DJ | |
dc.contributor.author | McMorran, BJ | |
dc.contributor.author | Foote, SJ | |
dc.contributor.author | Burgio, G | |
dc.date.accessioned | 2022-10-11T00:29:29Z | |
dc.date.available | 2019-04-08 | |
dc.date.available | 2022-10-11T00:29:29Z | |
dc.date.issued | 2019-04-23 | |
dc.identifier.citation | Sci Rep, 2019, 9, (1), pp. 6356 | |
dc.identifier.issn | 2045-2322 | |
dc.identifier.issn | 2045-2322 | |
dc.identifier.uri | http://hdl.handle.net/10453/162450 | |
dc.description.abstract | Plasmodium falciparum malaria causes half a million deaths per year, with up to 9% of this mortality caused by cerebral malaria (CM). One of the major processes contributing to the development of CM is an excess of host inflammatory cytokines. Recently K+ signaling has emerged as an important mediator of the inflammatory response to infection; we therefore investigated whether mice carrying an ENU induced activation of the electroneutral K+ channel KCC1 had an altered response to Plasmodium berghei. Here we show that Kcc1M935K/M935K mice are protected from the development of experimental cerebral malaria, and that this protection is associated with an increased CD4+ and TNFa response. This is the first description of a K+ channel affecting the development of experimental cerebral malaria. | |
dc.format | Electronic | |
dc.language | eng | |
dc.publisher | NATURE PUBLISHING GROUP | |
dc.relation.ispartof | Sci Rep | |
dc.relation.isbasedon | 10.1038/s41598-019-42782-x | |
dc.rights | info:eu-repo/semantics/openAccess | |
dc.subject.mesh | Animals | |
dc.subject.mesh | CD4-Positive T-Lymphocytes | |
dc.subject.mesh | CD8-Positive T-Lymphocytes | |
dc.subject.mesh | Cytokines | |
dc.subject.mesh | Disease Resistance | |
dc.subject.mesh | Female | |
dc.subject.mesh | Inflammation Mediators | |
dc.subject.mesh | Ion Channel Gating | |
dc.subject.mesh | Malaria, Cerebral | |
dc.subject.mesh | Male | |
dc.subject.mesh | Mice, Inbred BALB C | |
dc.subject.mesh | Mice, Inbred C57BL | |
dc.subject.mesh | Mutation | |
dc.subject.mesh | Plasmodium berghei | |
dc.subject.mesh | Solute Carrier Family 12, Member 4 | |
dc.subject.mesh | CD4-Positive T-Lymphocytes | |
dc.subject.mesh | CD8-Positive T-Lymphocytes | |
dc.subject.mesh | Animals | |
dc.subject.mesh | Mice, Inbred BALB C | |
dc.subject.mesh | Mice, Inbred C57BL | |
dc.subject.mesh | Plasmodium berghei | |
dc.subject.mesh | Malaria, Cerebral | |
dc.subject.mesh | Inflammation Mediators | |
dc.subject.mesh | Cytokines | |
dc.subject.mesh | Ion Channel Gating | |
dc.subject.mesh | Mutation | |
dc.subject.mesh | Female | |
dc.subject.mesh | Male | |
dc.subject.mesh | Disease Resistance | |
dc.subject.mesh | Solute Carrier Family 12, Member 4 | |
dc.title | KCC1 Activation protects Mice from the Development of Experimental Cerebral Malaria. | |
dc.type | Journal Article | |
utslib.citation.volume | 9 | |
utslib.location.activity | England | |
pubs.organisational-group | /University of Technology Sydney | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science/School of Life Sciences | |
utslib.copyright.status | open_access | * |
dc.date.updated | 2022-10-11T00:28:38Z | |
pubs.issue | 1 | |
pubs.publication-status | Published online | |
pubs.volume | 9 | |
utslib.citation.issue | 1 |
Abstract:
Plasmodium falciparum malaria causes half a million deaths per year, with up to 9% of this mortality caused by cerebral malaria (CM). One of the major processes contributing to the development of CM is an excess of host inflammatory cytokines. Recently K+ signaling has emerged as an important mediator of the inflammatory response to infection; we therefore investigated whether mice carrying an ENU induced activation of the electroneutral K+ channel KCC1 had an altered response to Plasmodium berghei. Here we show that Kcc1M935K/M935K mice are protected from the development of experimental cerebral malaria, and that this protection is associated with an increased CD4+ and TNFa response. This is the first description of a K+ channel affecting the development of experimental cerebral malaria.
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