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J Biol Chem, Vol. 274, Issue 27, 18872-18879, July 2, 1999
From the Departments of Salivary histatins are potent in
vitro antifungal proteins and have promise as therapeutic agents
against oral candidiasis. We performed pharmacological studies directed
at understanding the biochemical basis of Hst 5 candidacidal activity.
Three inhibitors of mitochondrial metabolism: carbonyl cyanide
p-chlorophenylhydrazone, dinitrophenol, and azide inhibited
Hst 5 killing of Candida albicans, while not inhibiting
cellular ATP production. In contrast, Hst 5 caused a drastic reduction
of C. albicans intracellular ATP content, which was a
result of an efflux of ATP. Carbonyl cyanide p-chlorophenylhydrazone, dinitrophenol, and azide inhibited
Hst 5-induced ATP efflux, thus establishing a correlation between ATP
release and cell killing. Furthermore, C. albicans cells
were respiring and had polarized membranes at least 80 min after ATP release, thus implying a non-lytic exit of cellular ATP in response to
Hst 5. Based on evidence that transmembrane ATP efflux can occur in the
absence of cytolysis through a channel-like pathway and that released
ATP can act as a cytotoxic mediator by binding to membrane purinergic
receptors, we evaluated whether extracellular ATP released by Hst 5 may
have further functional role in cell killing. Consistent with this
hypothesis, purinergic agonists BzATP and adenosine
5'O-(thiotriphosphate) induced loss of C. albicans cell viability and purinergic antagonists prevented Hst 5 killing.
Salivary Histatin 5 Induces Non-lytic Release of ATP from
Candida albicans Leading to Cell Death
,,, and§
Oral Biology and
§ Restorative Dentistry, School of Dental Medicine, State
University of New York at Buffalo, Buffalo, New York 14214
Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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