Hortle, ElinorStarrs, LoraBrown, Fiona G.Jane, Sephen MCurtis, David JMcMorran, BrendanFoote, SimonBurgio, Gaetan2022-11-292022-11-292045-2322http://hdl.handle.net/1885/281320Plasmodium 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.We would like to acknowledge Shelley Lampkin and Australian Phenomics Facility (APF) for the maintenance of the mouse colonies. Tis study was funded by the National Health and Medical Research Council of Australia (Program Grant 490037, and Project Grants 605524 and APP1047090), the National Collaborative Research Infrastructure Strategy (NCRIS), the Education Investment Fund from the Department of Education and Training, the Australian Phenomics Network, Howard Hughes Medical Institute and the Bill and Melinda Gates Foundation.application/pdfen-AU© The Author(s) 2019https://creativecommons.org/licenses/by/4.0/201910.1038/s41598-019-42782-x2021-11-28Creative Commons Attribution 4.0 International License