This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Hilger, A E Articles by Danley, D L Search for Related Content PubMed PubMed Citation Articles by Hilger, A E Articles by Danley, D L

 Previous Article  |  Next Article 

Infect Immun. 1980 March; 27(3): 714-720

Alteration of polymorphonuclear leukocyte activity by viable Candida albicans.

ABSTRACT

The response of human polymorphonuclear leukocytes (PMN) to blastospores and pseudo-hyphae of the opportunistic fungus Candida albicans has been studied in vitro and in vivo. Of the fungicidal mechanisms elucidated thus far, the myeloperoxidase-hydrogen peroxide-halide system appears to be most effective against cells of this fungus. In our studies on the interaction between murine PMN and blastospores, we assayed the release of H2O2 by PMN incubated with viable or killed, unopsonized or opsonized blastospores by using two assay systems, lysis of murine erythrocytes and oxidation of scopoletin. Our results showed that PMN released increasing amounts of H2O2 when incubated with increasing numbers of opsonized or unopsonized killed blastospores, but released decreasing amounts of H2O2 when incubated with increasing numbers of opsonized or unopsonized viable blastospores. The oxidative metabolic burst by PMN in the presence of viable or killed blastospores was also measured by using reduction of nitroblue tetrazolium and chemiluminescence. Viable blastospores stimulated a stronger metabolic burst than killed blastospores, suggesting that PMN respond to live blastospores more vigorously than killed blastospores; however, live blastospores appear to alter or inhibit the release of H2O2 by PMN.

This article has been cited by other articles:

• Finkel-Jimenez, B., Wuthrich, M., Klein, B. S. (2002). BAD1, an Essential Virulence Factor of Blastomyces dermatitidis, Suppresses Host TNF-{alpha} Production Through TGF-{beta}-Dependent and -Independent Mechanisms. J. Immunol. 168: 5746-5755 [Abstract] [Full Text]  
• Finkel-Jimenez, B., Wuthrich, M., Brandhorst, T., Klein, B. S. (2001). The WI-1 Adhesin Blocks Phagocyte TNF-{{alpha}} Production, Imparting Pathogenicity on Blastomyces dermatitidis. J. Immunol. 166: 2665-2673 [Abstract] [Full Text]