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KCC1 Activation protects Mice from the Development of Experimental Cerebral Malaria

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 mediat...

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Detalles Bibliográficos
Autores principales: Hortle, Elinor, Starrs, Lora, Brown, Fiona C., Jane, Stephen M., Curtis, David J., McMorran, Brendan J., Foote, Simon J., Burgio, Gaetan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6478876/
https://www.ncbi.nlm.nih.gov/pubmed/31015511
http://dx.doi.org/10.1038/s41598-019-42782-x
Descripción
Sumario: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 Kcc1(M935K/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.