TY - JOUR
T1 - Interactions between human phagocytes and candida albicans biofilms alone and in combination with antifungal agents
AU - Katragkou, Aspasia
AU - Kruhlak, Michael J.
AU - Simitsopoulou, Maria
AU - Chatzimoschou, Athanasios
AU - Taparkou, Anna
AU - Cotten, Catherine J.
AU - Paliogianni, Fotini
AU - Diza-Mataftsi, Eudoxia
AU - Tsantali, Chaido
AU - Walsh, Thomas J.
AU - Roilides, Emmanuel
N1 - Funding Information:
Financial support: This study was partially supported by Aristotle University, Thessaloniki, Greece, and the intramural research program of the National Cancer Institute, Bethesda, Maryland. A.K. was a recipient of a grant from the European Society of Pediatric Infectious Diseases (2006–2007 Small Grant Awards) and a grant from Pfizer (GA900095).
PY - 2010/6/15
Y1 - 2010/6/15
N2 - Background. Biofilm formation is an important component of vascular catheter infections caused by Candida albicans. Little is known about the interactions between human phagocytes, antifungal agents, and Candida biofilms. Methods. The interactions between C. albicans biofilms and human phagocytes alone and in combination with anidulafungin or voriconazole were investigated and compared with their corresponding planktonic counterparts by means of an in vitro biofilm model with clinical intravascular and green fluorescent protein (GFP)-expressing strains. Phagocyte-mediated and antifungal agent-mediated damages were determined by 2,3-bis[2-methoxy-4nitro-5-sulfophenyl]2H- tetrazolium-5-carboxanilide assay, and structural effects were visualized by confocal microscopy. Oxidative burst was evaluated by flow cytometric measurement of dihydrorhodamine 123 oxidation, and cytokine release was measured by enzyme-linked immunosorbent assay. Results. Phagocytes alone and in combination with antifungal agents induced less damage against biofilms compared with planktonic cells. However, additive effects occurred between phagocytes and anidulafungin against Candida biofilms. Confocal microscopy demonstrated the absence of phagocytosis within biofilms but marked destruction caused by anidulafungin and phagocytes. Anidulafungin but not voriconazole elicited tumor necrosis factor a release from phagocytes compared with that from untreated biofilms. Conclusions. C. albicans within biofilms are more resistant to phagocytic host defenses but are susceptible to additive effects between phagocytes and an echinocandin.
AB - Background. Biofilm formation is an important component of vascular catheter infections caused by Candida albicans. Little is known about the interactions between human phagocytes, antifungal agents, and Candida biofilms. Methods. The interactions between C. albicans biofilms and human phagocytes alone and in combination with anidulafungin or voriconazole were investigated and compared with their corresponding planktonic counterparts by means of an in vitro biofilm model with clinical intravascular and green fluorescent protein (GFP)-expressing strains. Phagocyte-mediated and antifungal agent-mediated damages were determined by 2,3-bis[2-methoxy-4nitro-5-sulfophenyl]2H- tetrazolium-5-carboxanilide assay, and structural effects were visualized by confocal microscopy. Oxidative burst was evaluated by flow cytometric measurement of dihydrorhodamine 123 oxidation, and cytokine release was measured by enzyme-linked immunosorbent assay. Results. Phagocytes alone and in combination with antifungal agents induced less damage against biofilms compared with planktonic cells. However, additive effects occurred between phagocytes and anidulafungin against Candida biofilms. Confocal microscopy demonstrated the absence of phagocytosis within biofilms but marked destruction caused by anidulafungin and phagocytes. Anidulafungin but not voriconazole elicited tumor necrosis factor a release from phagocytes compared with that from untreated biofilms. Conclusions. C. albicans within biofilms are more resistant to phagocytic host defenses but are susceptible to additive effects between phagocytes and an echinocandin.
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U2 - 10.1086/652783
DO - 10.1086/652783
M3 - Article
C2 - 20415537
AN - SCOPUS:77952559259
SN - 0022-1899
VL - 201
SP - 1941
EP - 1949
JO - Journal of Infectious Diseases
JF - Journal of Infectious Diseases
IS - 12
ER -