Immunopathogenesis of Oropharyngeal Candidiasis in Human Immunodeficiency Virus Infection

Repentigny, Louis de; Lewandowski, Daniel; Jolicoeur, Paul

doi:10.1128/cmr.17.4.729-759.2004

Cited by 197 publications

(217 citation statements)

References 465 publications

(555 reference statements)

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“…Thus, the model closely reproduces the mucosal candidiasis found in HIV/AIDS patients. Indeed, among these patients, esophagus and GI tract are strongly colonized while systemic dissemination rarely occurs (27,28). Our results in RAG-2 Ϫ/Ϫ mice are in line with other studies using SCID mice.…”

Section: Discussionmentioning

confidence: 99%

IL-13 Attenuates Gastrointestinal Candidiasis in Normal and Immunodeficient RAG-2−/− Mice via Peroxisome Proliferator-Activated Receptor-γ Activation

Coste

Lagane

Filipe

et al. 2008

The Journal of Immunology

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We recently demonstrated that in vitro peroxisome proliferator-activated receptor-γ (PPARγ) activation of mouse peritoneal macrophages by IL-13 or PPARγ ligands promotes uptake and killing of Candida albicans through mannose receptor overexpression. In this study, we demonstrate that i.p. treatment of immunocompetent and immunodeficient (RAG-2−/−) mice with natural and synthetic PPARγ-specific ligands or with IL-13 decreases C. albicans colonization of the gastrointestinal (GI) tract 8 days following oral infection with the yeast. We also showed that Candida GI infection triggers macrophage recruitment in cecum mucosa. These mucosal macrophages, as well as peritoneal macrophages, overexpress the mannose receptor after IL-13 and rosiglitazone treatments. The treatments promote macrophage activation against C. albicans as suggested by the increased ability of peritoneal macrophages to phagocyte C. albicans and to produce reactive oxygen intermediates after yeast challenge. These effects on C. albicans GI infection and on macrophage activation are suppressed by treatment of mice with GW9662, a selective PPARγ antagonist, and are reduced in PPARγ+/− mice. Overall, these data demonstrate that IL-13 or PPARγ ligands attenuate C. albicans infection of the GI tract through PPARγ activation and hence suggest that PPARγ ligands may be of therapeutic value in esophageal and GI candidiasis in immunocompromised patients.

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Section: Discussionmentioning

confidence: 99%

IL-13 Attenuates Gastrointestinal Candidiasis in Normal and Immunodeficient RAG-2−/− Mice via Peroxisome Proliferator-Activated Receptor-γ Activation

Coste

Lagane

Filipe

et al. 2008

The Journal of Immunology

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“…However, under conditions of immune disruption, C. albicans can rapidly transition into a pathogen, causing an array of mucosal and disseminated infections with high mortality (de Repentigny et al, 2004). As a polymorphic species, C. albicans is capable of switching morphology between yeast and hyphal forms, a transition crucial to its pathogenesis.…”

Section: Introductionmentioning

confidence: 99%

Staphylococcus aureus adherence to Candida albicans hyphae is mediated by the hyphal adhesin Als3p

et al. 2012

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The bacterium Staphylococcus (St.) aureus and the opportunistic fungus Candida albicans are currently among the leading nosocomial pathogens, often co-infecting critically ill patients, with high morbidity and mortality. Previous investigations have demonstrated preferential adherence of St. aureus to C. albicans hyphae during mixed biofilm growth. In this study, we aimed to characterize the mechanism behind this observed interaction. C. albicans adhesin-deficient mutant strains were screened by microscopy to identify the specific receptor on C. albicans hyphae recognized by St. aureus. Furthermore, an immunoassay was developed to validate and quantify staphylococcal binding to fungal biofilms. The findings from these experiments implicated the C. albicans adhesin agglutinin-like sequence 3 (Als3p) in playing a major role in the adherence process. This association was quantitatively established using atomic force microscopy, in which the adhesion force between single cells of the two species was significantly reduced for a C. albicans mutant strain lacking als3. Confocal microscopy further confirmed these observations, as St. aureus overlaid with a purified recombinant Als3 N-terminal domain fragment (rAls3p) exhibited robust binding. Importantly, a strain of Saccharomyces cerevisiae heterologously expressing Als3p was utilized to further confirm this adhesin as a receptor for St. aureus. Although the parental strain does not bind bacteria, expression of Als3p on the cell surface conferred upon the yeast the ability to strongly bind St. aureus. To elucidate the implications of these in vitro findings in a clinically relevant setting, an ex vivo murine model of co-infection was designed using murine tongue explants. Fluorescent microscopic images revealed extensive hyphal penetration of the epithelium typical of C. albicans mucosal infection. Interestingly, St. aureus bacterial cells were only seen within the Abbreviations: AFM, atomic force microscopy; CLSM, confocal laser scanning microscopy; ConA-Texas red, concanavalin A conjugated to Texas red; H&E, haematoxylin and eosin; IFA, indirect immunofluorescence; PNA-FISH, peptide nucleic acid probes for fluorescent in situ hybridization; SEM, scanning electron microscopy. A supplementary figure is available with the online version of this paper. Microbiology

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“…Histatin proteins demonstrate broad spectrum antifungal activity against pathogenic fungi like Candida spp, Cryptococcus neoformans and Aspergillus fumigatus [10]. Edgerton et al [11] reported anti candidal activity of histatin 5.…”

Section: Innate Immunitymentioning

confidence: 99%

“…In addition, it also damages the fungal cell wall and activates intracellular autolytic enzymes [10].…”

Section: Innate Immunitymentioning

confidence: 99%

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Immunity to Candida Infection: An Overview

Deorukhkar¹

2017

MOJI

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Candida is found as a commensal of gastrointestinal and genital tract. However in contrast to many other commensals, Candida possesses a prominent ability to invade any tissue of a host presenting with innate or acquired immune deficiency. Candida spp. is an opportunistic pathogen that has acquainted various virulence traits facilitating host tissue colonization and invasion, and impairment of host defenses. The immune system is a remarkably versatile defense system that protects an individual from invasion of pathogens including Candida. Host defense mechanisms against candidiasis involve activation of an acute inflammatory response by innate immunity, followed by specific T cell (cell mediated immunity) or B cell (humoral immunity) mediated immune responses.

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Immunopathogenesis of Oropharyngeal Candidiasis in Human Immunodeficiency Virus Infection

Cited by 197 publications

References 465 publications

IL-13 Attenuates Gastrointestinal Candidiasis in Normal and Immunodeficient RAG-2−/− Mice via Peroxisome Proliferator-Activated Receptor-γ Activation

IL-13 Attenuates Gastrointestinal Candidiasis in Normal and Immunodeficient RAG-2−/− Mice via Peroxisome Proliferator-Activated Receptor-γ Activation

Staphylococcus aureus adherence to Candida albicans hyphae is mediated by the hyphal adhesin Als3p

Immunity to Candida Infection: An Overview

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