Zebrafish as a Model Host for
            <i>Candida albicans</i>
            Infection

Chao, Chun‐Cheih; Hsu, Po-Chen; Jen, Chung-Feng; Chen, I-Hui; Wang, Chieh-Huei; Chan, Hau-Chien; Tsai, Pei-Wen; Tung, Ken; Wang, Chian-Huei; Lan, Chung-Yu; Chuang, Yung-Jen

doi:10.1128/iai.01293-09

Cited by 97 publications

(90 citation statements)

References 49 publications

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“…They found that the C. albicans induced mortalities among adult zebrafish in a dose-dependent manner. Moreover, histopathological findings revealed that C. albicans colonized multiple anatomical sites in the adult zebrafish (Chao et al, 2010). Epithelial cells play an important role in signaling specific cells to support an immune response to C. albicans (Gratacap et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

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Oda¹,

Tohamy²,

Massoud³

2016

Turk. J. Fish. Aquat. Sci.

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This study was performed to investigate the alterations that associated with experimental infection of Nile tilapia with Streptococcus iniae (S. iniae), Candida albicans (C. albicans) or their combination. The experimentally infected fish were carefully observed for four weeks for any clinical abnormalities, mortality rates, postmortem changes, biochemical and histopathological changes. The highest mortality rate, severe clinical signs and postmortem changes occurred in Nile tilapia fish in the S. iniae+ C. albicans infected group. There were significant changes in the evaluated biochemical parameters in all infected groups that were marked in the S. iniae-and the S. iniae+ C. albicans-infected groups. Specimens were collected from gills, liver, kidney, spleen, brain and intestine for histopathological examination. The lesions were variable among the infected groups, however; lesions intensity was more pronounced in fish infected with both pathogens. The present study established the synergistic interaction between S. iniae and C. albicans in Nile tilapia on the bases of clinical signs, mortality rates, postmortem changes, biochemical and histopathological changes.

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Section: Discussionmentioning

confidence: 99%

“…It also acts as a source of human infection (Calderone, 2002). Chao et al, 2010 assessed the use of zebrafish as a host model to study the pathogenicity of invasive C. albicans. They found that the C. albicans induced mortalities among adult zebrafish in a dose-dependent manner.…”

Section: Discussionmentioning

confidence: 99%

Untitled

Oda¹,

Tohamy²,

Massoud³

2016

Turk. J. Fish. Aquat. Sci.

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“…rected gene knockdown, both of which are techniques available with the larval host (19). Also, while others have described a localized embryonic zebrafish infection model (19), it is not clear if and how these infections parallel human diseases of clinical importance, such as disseminated candidiasis.…”

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confidence: 99%

Live Imaging of Disseminated Candidiasis in Zebrafish Reveals Role of Phagocyte Oxidase in Limiting Filamentous Growth

2011

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Candida albicans is a human commensal and a clinically important fungal pathogen that grows in both yeast and hyphal forms during human infection. Although Candida can cause cutaneous and mucosal disease, systemic infections cause the greatest mortality in hospitals. Candidemia occurs primarily in immunocompromised patients, for whom the innate immune system plays a paramount role in immunity. We have developed a novel transparent vertebrate model of candidemia to probe the molecular nature of Candida-innate immune system interactions in an intact host. Our zebrafish infection model results in a lethal disseminated disease that shares important traits with disseminated candidiasis in mammals, including dimorphic fungal growth, dependence on hyphal growth for virulence, and dependence on the phagocyte NADPH oxidase for immunity. Dual imaging of fluorescently marked immune cells and fungi revealed that phagocytosed yeast cells can remain viable and even divide within macrophages without germinating. Similarly, although we observed apparently killed yeast cells within neutrophils, most yeast cells within these innate immune cells were viable. Exploiting this model, we combined intravital imaging with gene knockdown to show for the first time that NADPH oxidase is required for regulation of C. albicans filamentation in vivo. The transparent and easily manipulated larval zebrafish model promises to provide a unique tool for dissecting the molecular basis of phagocyte NADPH oxidase-mediated limitation of filamentous growth in vivo.Candida albicans is a human commensal that causes lifethreatening invasive infections in immunocompromised patients. Disseminated candidiasis is the 4th leading infection in hospitalized patients in the United States, and despite antifungal therapy, the mortality associated with candidemia can reach 30 to 40% (62). Innate immunity is a key mediator of resistance to disseminated infection in both mice and humans, and defects in professional innate immune cells predispose individuals to invasive candidemia (5,26,68).The zebrafish larva is a unique and powerful model for noninvasively visualizing and understanding the interactions of pathogens with the innate immune system (17,48,56). Notably, zebrafish have similar signaling through Toll-like receptors to that in humans, express similar cytokines, and have macrophages, neutrophils, dendritic cells, mast cells, eosinophils, T cells, and B cells (78). The delayed development of T cells and B cells, which do not mature until approximately 30 days postfertilization, permits a natural focus on innate immunity in embryonic and larval infection models. A larval model of candidemia offers several advantages compared to other recently described models of zebrafish infection with C. albicans. Specifically, the adult zebrafish candidemia model does not permit real-time visualization of infection or morpholino (MO)-directed gene knockdown, both of which are techniques available with the larval host (19). Also, while others have described a localized embry...

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“…The embryonic zebrafish (Danio rerio) has a number of advantages as a model that makes it an increasingly attractive vertebrate host in which to study infectious disease (11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24). The zebrafish is genetically tractable with a sequenced genome (http://www.sanger.ac.uk/Projects/D_rerio/) and is amenable to forward and reverse genetic screens.…”

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confidence: 99%

Innate Immune Response to Streptococcus iniae Infection in Zebrafish Larvae

et al. 2013

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dStreptococcus iniae causes systemic infection characterized by meningitis and sepsis. Here, we report a larval zebrafish model of S. iniae infection. Injection of wild-type S. iniae into the otic vesicle induced a lethal infection by 24 h postinfection. In contrast, an S. iniae mutant deficient in polysaccharide capsule (cpsA mutant) was not lethal, with greater than 90% survival at 24 h postinfection. Live imaging demonstrated that both neutrophils and macrophages were recruited to localized otic infection with mutant and wild-type S. iniae and were able to phagocytose bacteria. Depletion of neutrophils and macrophages impaired host survival following infection with wild-type S. iniae and the cpsA mutant, suggesting that leukocytes are critical for host survival in the presence of both the wild-type and mutant bacteria. However, zebrafish larvae with impaired neutrophil function but normal macrophage function had increased susceptibility to wild-type bacteria but not the cpsA mutant. Taking these findings together, we have developed a larval zebrafish model of S. iniae infection and have found that although neutrophils are important for controlling infection with wild-type S. iniae, neutrophils are not necessary for host defense against the cpsA mutant.

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Zebrafish as a Model Host for Candida albicans Infection

Cited by 97 publications

References 49 publications

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Live Imaging of Disseminated Candidiasis in Zebrafish Reveals Role of Phagocyte Oxidase in Limiting Filamentous Growth

Innate Immune Response to Streptococcus iniae Infection in Zebrafish Larvae

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