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Research - Candida & Gut Dysbiosis Research

 

 

Antimicrob Agents Chemother. 2008 Aug 18. [Epub ahead of print]

 

Human lactoferrin induces apoptosis-like cell death in Candida albicans: Critical role of K+-channel-mediated K+-efflux.

 

Andrés MT, Viejo-Díaz M, Fierro JF. Laboratory of Oral Microbiology. School of Stomatology, and Department of Functional Biology (Microbiology). Faculty of Medicine. University of Oviedo. 33006 Oviedo. Spain.

 

 

Human lactoferrin (hLf) induced an apoptosis-like phenotype in Candida albicans cells, which includes phosphatidylserine externalization, nuclear chromatin condensation, DNA degradation, and increased reactive oxygen species (ROS) production. Intracellular ROS accumulation was seen to correlate with candidacidal activity in hLf-treated cells. Mitochondrial activity was involved as indicated by mitochondrial depolarization and increased hLf-resistance of cells preincubated with sordarin or erythromycin, the latter of which inhibits protein synthesis in mitoribosomes. Interestingly, Cl(-)- and K(+)-channel blockers prevented the hLf-antimicrobial activity, but only when cells were pretreated with the blocking agent (TEA) prior to the hLf-induced K(+)-release period. These results indicate for the first time that K(+)-channel-mediated K(+)-efflux is required for the progression of apoptosis-like process in yeast, suggesting that this essential apoptotic event of higher-eukaryotes has been evolutionary conserved among species ranging from yeast to man.

 

PMID: 18710913 [PubMed - as supplied by publisher]

 

 

 

 

 

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