Histatin 5 killing activity studied in candida albicans
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Histatins are a group of histidine-rich proteins present in human salivary secretions. They exhibit antimicrobial activity, and therefore are considered to be important in the oral cavity, specifically in the prevention of infections with the opportunistic pathogen Candida albocans albicans. Although killing of both blastoconidia and germ tubes of C. albicans by histatins has been extensively studied, little is known about the processes responsible for this antifungal activity. Therefore, to determine the cellular localization and the kinetics of histatin interaction with C. albicans, synthetic histatin 5 was labeled with fluorescein-5-isothiocyanate (FITC), and uptake was followed by epifluorescence and confocal microscopy. Uptake of FITC-histatin 5 was rapid and time-dependent at 37 degree C, and maximum fluorescence was detected in the cytoplasm of both blastoconidia and gem tubes after 60 min. Similarly, killing of blastoconidia and germ tubes was also maximal after incubation with histatin 5 for 60 min. The correlation between histatin 5 killing activity and intracellular accumulation suggested that histatin 5 may exert its lethal effect via an intracellular target. Differential centrifugation of cell lysates showed that histatin 5 accumulated preferentially in preparations enriched with mitochondria and endoplasmic reticulum. These findings suggested that uptake of histatin 5 could be correlated with killing activity, and provided insights into the mechanism of candidacidal activity. Interestingly, when killing and uptake experiments were carried out at 4 degree C, neither intracellular accumulation of FITC-labeled histatin 5 nor killing activity was observed. [TRUNCATED]
PLEASE NOTE: This work is protected by copyright. Downloading is restricted to the BU community: please click Download and log in with a valid BU account to access. If you are the author of this work and would like to make it publicly available, please contact firstname.lastname@example.org.Thesis (D.Sc.D.)--Boston University, Henry M. Goldman School of Dental Medicine, 1999 (Oral Biology).Includes bibliographical references (leaves 191-213).
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