Purpurin triggers caspase-independent apoptosis in Candida dubliniensis biofilms
Candida dubliniensis is an important human fungal pathogen that causes oral infections in patients with AIDS and diabetes mellitus. However, C. Dubliniensis has been frequently reported in bloodstream infections in clinical settings. Like its phylogenetically related virulent species C. albicans, C....
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description | Candida dubliniensis is an important human fungal pathogen that causes oral infections in patients with AIDS and diabetes mellitus. However, C. Dubliniensis has been frequently reported in bloodstream infections in clinical settings. Like its phylogenetically related virulent species C. albicans, C. Dubliniensis is able to grow and switch between yeast form and filamentous form (hyphae) and develops biofilms on both abiotic and biotic surfaces. Biofilms are recalcitrant to antifungal therapies and C. Dubliniensis readily turns drug resistant upon repeated exposure. More than 80% of infections are associated with biofilms. Suppression of fungal biofilms may therefore represent a viable antifungal strategy with clinical relevance. Here, we report that C. dubliniensis biofilms were inhibited by purpurin, a natural anthraquinone pigment isolated from madder root. Purpurin inhibited C. dubliniensis biofilm formation in a concentration-dependent manner; while mature biofilms were less susceptible to purpurin. Scanning electron microscopy (SEM) analysis revealed scanty structure consisting of yeast cells in purpurin-treated C. dubliniensis biofilms. We sought to delineate the mechanisms of the anti-biofilm activity of purpurin on C. Dubliniensis. Intracellular ROS levels were significantly elevated in fungal biofilms and depolarization of MMP was evident upon purpurin treatment in a concentration-dependent manner. DNA degradation was evident. However, no activated metacaspase could be detected. Together, purpurin triggered metacaspase-independent apoptosis in C. dubliniensis biofilms. |
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However, C. Dubliniensis has been frequently reported in bloodstream infections in clinical settings. Like its phylogenetically related virulent species C. albicans, C. Dubliniensis is able to grow and switch between yeast form and filamentous form (hyphae) and develops biofilms on both abiotic and biotic surfaces. Biofilms are recalcitrant to antifungal therapies and C. Dubliniensis readily turns drug resistant upon repeated exposure. More than 80% of infections are associated with biofilms. Suppression of fungal biofilms may therefore represent a viable antifungal strategy with clinical relevance. Here, we report that C. dubliniensis biofilms were inhibited by purpurin, a natural anthraquinone pigment isolated from madder root. Purpurin inhibited C. dubliniensis biofilm formation in a concentration-dependent manner; while mature biofilms were less susceptible to purpurin. Scanning electron microscopy (SEM) analysis revealed scanty structure consisting of yeast cells in purpurin-treated C. dubliniensis biofilms. We sought to delineate the mechanisms of the anti-biofilm activity of purpurin on C. Dubliniensis. Intracellular ROS levels were significantly elevated in fungal biofilms and depolarization of MMP was evident upon purpurin treatment in a concentration-dependent manner. DNA degradation was evident. However, no activated metacaspase could be detected. Together, purpurin triggered metacaspase-independent apoptosis in C. dubliniensis biofilms.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0086032</identifier><identifier>PMID: 24376900</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Acquired immune deficiency syndrome ; AIDS ; Analysis ; Anthraquinone ; Anthraquinones - pharmacology ; Antifungal agents ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - physiology ; Biodegradation ; Biofilms ; Biofilms - drug effects ; Candida ; Candida - drug effects ; Candida - physiology ; Candida - ultrastructure ; Candida albicans ; Candida krusei ; Caspase ; Cross infection ; Dentistry ; Deoxyribonucleic acid ; Depolarization ; Diabetes mellitus ; DNA ; Drug resistance ; Drug Resistance, Fungal - physiology ; Electron microscopy ; Fungi ; Fungicides ; Gene expression ; Health aspects ; Hyphae ; In Situ Nick-End Labeling ; Infections ; Metabolism ; Microscopy, Electron, Scanning ; Mitochondria ; Nosocomial infections ; Pathogens ; Phylogeny ; Reactive Oxygen Species - metabolism ; Scanning electron microscopy ; Statistics, Nonparametric ; Yeast</subject><ispartof>PloS one, 2013-12, Vol.8 (12), p.e86032-e86032</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Tsang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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However, C. Dubliniensis has been frequently reported in bloodstream infections in clinical settings. Like its phylogenetically related virulent species C. albicans, C. Dubliniensis is able to grow and switch between yeast form and filamentous form (hyphae) and develops biofilms on both abiotic and biotic surfaces. Biofilms are recalcitrant to antifungal therapies and C. Dubliniensis readily turns drug resistant upon repeated exposure. More than 80% of infections are associated with biofilms. Suppression of fungal biofilms may therefore represent a viable antifungal strategy with clinical relevance. Here, we report that C. dubliniensis biofilms were inhibited by purpurin, a natural anthraquinone pigment isolated from madder root. Purpurin inhibited C. dubliniensis biofilm formation in a concentration-dependent manner; while mature biofilms were less susceptible to purpurin. Scanning electron microscopy (SEM) analysis revealed scanty structure consisting of yeast cells in purpurin-treated C. dubliniensis biofilms. We sought to delineate the mechanisms of the anti-biofilm activity of purpurin on C. Dubliniensis. Intracellular ROS levels were significantly elevated in fungal biofilms and depolarization of MMP was evident upon purpurin treatment in a concentration-dependent manner. DNA degradation was evident. However, no activated metacaspase could be detected. Together, purpurin triggered metacaspase-independent apoptosis in C. dubliniensis biofilms.</description><subject>Acquired immune deficiency syndrome</subject><subject>AIDS</subject><subject>Analysis</subject><subject>Anthraquinone</subject><subject>Anthraquinones - pharmacology</subject><subject>Antifungal agents</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - physiology</subject><subject>Biodegradation</subject><subject>Biofilms</subject><subject>Biofilms - drug effects</subject><subject>Candida</subject><subject>Candida - drug effects</subject><subject>Candida - physiology</subject><subject>Candida - ultrastructure</subject><subject>Candida albicans</subject><subject>Candida krusei</subject><subject>Caspase</subject><subject>Cross infection</subject><subject>Dentistry</subject><subject>Deoxyribonucleic acid</subject><subject>Depolarization</subject><subject>Diabetes mellitus</subject><subject>DNA</subject><subject>Drug resistance</subject><subject>Drug Resistance, Fungal - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tsang, Paul Wai-Kei</au><au>Wong, Alan Pak-Kin</au><au>Yang, Hai-Ping</au><au>Li, Ngai-For</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Purpurin triggers caspase-independent apoptosis in Candida dubliniensis biofilms</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2013-12-23</date><risdate>2013</risdate><volume>8</volume><issue>12</issue><spage>e86032</spage><epage>e86032</epage><pages>e86032-e86032</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Candida dubliniensis is an important human fungal pathogen that causes oral infections in patients with AIDS and diabetes mellitus. However, C. Dubliniensis has been frequently reported in bloodstream infections in clinical settings. Like its phylogenetically related virulent species C. albicans, C. Dubliniensis is able to grow and switch between yeast form and filamentous form (hyphae) and develops biofilms on both abiotic and biotic surfaces. Biofilms are recalcitrant to antifungal therapies and C. Dubliniensis readily turns drug resistant upon repeated exposure. More than 80% of infections are associated with biofilms. Suppression of fungal biofilms may therefore represent a viable antifungal strategy with clinical relevance. Here, we report that C. dubliniensis biofilms were inhibited by purpurin, a natural anthraquinone pigment isolated from madder root. Purpurin inhibited C. dubliniensis biofilm formation in a concentration-dependent manner; while mature biofilms were less susceptible to purpurin. Scanning electron microscopy (SEM) analysis revealed scanty structure consisting of yeast cells in purpurin-treated C. dubliniensis biofilms. We sought to delineate the mechanisms of the anti-biofilm activity of purpurin on C. Dubliniensis. Intracellular ROS levels were significantly elevated in fungal biofilms and depolarization of MMP was evident upon purpurin treatment in a concentration-dependent manner. DNA degradation was evident. However, no activated metacaspase could be detected. Together, purpurin triggered metacaspase-independent apoptosis in C. dubliniensis biofilms.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24376900</pmid><doi>10.1371/journal.pone.0086032</doi><tpages>e86032</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Acquired immune deficiency syndrome AIDS Analysis Anthraquinone Anthraquinones - pharmacology Antifungal agents Apoptosis Apoptosis - drug effects Apoptosis - physiology Biodegradation Biofilms Biofilms - drug effects Candida Candida - drug effects Candida - physiology Candida - ultrastructure Candida albicans Candida krusei Caspase Cross infection Dentistry Deoxyribonucleic acid Depolarization Diabetes mellitus DNA Drug resistance Drug Resistance, Fungal - physiology Electron microscopy Fungi Fungicides Gene expression Health aspects Hyphae In Situ Nick-End Labeling Infections Metabolism Microscopy, Electron, Scanning Mitochondria Nosocomial infections Pathogens Phylogeny Reactive Oxygen Species - metabolism Scanning electron microscopy Statistics, Nonparametric Yeast |
title | Purpurin triggers caspase-independent apoptosis in Candida dubliniensis biofilms |
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