Expression of Secreted Aspartyl Proteinases in an Experimental Model of <i>Candida albicans</i>‐Associated Denture Stomatitis

Tobouti, Priscila Lie; Casaroto, Ana Regina; Almeida, Ricardo Sérgio; Ramos, Solange de Paula; Dionísio, Thiago José; Porto, Vinícius Carvalho; Santos, Carlos; Lara, Vanessa Soares

doi:10.1111/jopr.12285

Cited by 25 publications

(53 citation statements)

References 41 publications

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“…Rats also exhibited gradual worsening of erythematous palatal inflammation, while histopathology of the palate tissue revealed neutrophil infiltration, indicative of a strong inflammatory response (123). Using a similar rat model of DS, a separate study indicated that C. albicans SAP expression correlated with histological changes, suggesting that specific fungal virulence factors promote tissue damage (126).…”

Section: Non-cd4mentioning

confidence: 93%

Candida albicans Pathogenesis: Fitting within the Host-Microbe Damage Response Framework

et al. 2016

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f Historically, the nature and extent of host damage by a microbe were considered highly dependent on virulence attributes of the microbe. However, it has become clear that disease is a complex outcome which can arise because of pathogen-mediated damage, host-mediated damage, or both, with active participation from the host microbiota. This awareness led to the formulation of the damage response framework (DRF), a revolutionary concept that defined microbial virulence as a function of host immunity. The DRF outlines six classifications of host damage outcomes based on the microbe and the strength of the immune response. In this review, we revisit this concept from the perspective of Candida albicans, a microbial pathogen uniquely adapted to its human host. This fungus commonly colonizes various anatomical sites without causing notable damage. However, depending on environmental conditions, a diverse array of diseases may occur, ranging from mucosal to invasive systemic infections resulting in microbe-mediated and/or host-mediated damage. Remarkably, C. albicans infections can fit into all six DRF classifications, depending on the anatomical site and associated host immune response. Here, we highlight some of these diverse and site-specific diseases and how they fit the DRF classifications, and we describe the animal models available to uncover pathogenic mechanisms and related host immune responses.

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Section: Non-cd4mentioning

confidence: 93%

Candida albicans Pathogenesis: Fitting within the Host-Microbe Damage Response Framework

et al. 2016

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“…For obvious ethical and cost issues, rodent models were employed and were found to consistently reproduce clinical DS; therefore, the rat model is established as the gold standard to study biofilm-associated Candida DS. Several contemporary in vivo rat models of DS exist, each with their own specific indications, advantages, and limitations [63,76,[229][230][231]. Many of these models proved how closely the disease process in rats can mimic what is seen in humans.…”

Section: Rat Model Of Denture Stomatitismentioning

confidence: 99%

“…This is so because the clinical and histopathological changes of DS in several of these rat models are identical to what is seen in humans. Similar to the mouse models of OC, the rat models were also adapted and optimized for host immune response studies, gene expression studies, for studying mechanisms of Candida drug resistance, and for therapeutic evaluations [63,230]. However, one main disadvantage of these models is the method of retention used to secure the appliance to the rat palates, which involves tying orthodontic wires around the rat teeth [63,229,230].…”

Section: Rat Model Of Denture Stomatitismentioning

confidence: 99%

“…Similar to the mouse models of OC, the rat models were also adapted and optimized for host immune response studies, gene expression studies, for studying mechanisms of Candida drug resistance, and for therapeutic evaluations [63,230]. However, one main disadvantage of these models is the method of retention used to secure the appliance to the rat palates, which involves tying orthodontic wires around the rat teeth [63,229,230]. Although effective in retaining the appliances in the animals, the installation procedure is time-consuming, technically challenging, and likely causes discomfort to the animals.…”

Section: Rat Model Of Denture Stomatitismentioning

confidence: 99%

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Oral Candidiasis: A Disease of Opportunity

Vila

Sultan

Montelongo-Jauregui

et al. 2020

JoF

290

241

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Oral candidiasis, commonly referred to as “thrush,” is an opportunistic fungal infection that commonly affects the oral mucosa. The main causative agent, Candida albicans, is a highly versatile commensal organism that is well adapted to its human host; however, changes in the host microenvironment can promote the transition from one of commensalism to pathogen. This transition is heavily reliant on an impressive repertoire of virulence factors, most notably cell surface adhesins, proteolytic enzymes, morphologic switching, and the development of drug resistance. In the oral cavity, the co-adhesion of C. albicans with bacteria is crucial for its persistence, and a wide range of synergistic interactions with various oral species were described to enhance colonization in the host. As a frequent colonizer of the oral mucosa, the host immune response in the oral cavity is oriented toward a more tolerogenic state and, therefore, local innate immune defenses play a central role in maintaining Candida in its commensal state. Specifically, in addition to preventing Candida adherence to epithelial cells, saliva is enriched with anti-candidal peptides, considered to be part of the host innate immunity. The T helper 17 (Th17)-type adaptive immune response is mainly involved in mucosal host defenses, controlling initial growth of Candida and inhibiting subsequent tissue invasion. Animal models, most notably the mouse model of oropharyngeal candidiasis and the rat model of denture stomatitis, are instrumental in our understanding of Candida virulence factors and the factors leading to host susceptibility to infections. Given the continuing rise in development of resistance to the limited number of traditional antifungal agents, novel therapeutic strategies are directed toward identifying bioactive compounds that target pathogenic mechanisms to prevent C. albicans transition from harmless commensal to pathogen.

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“…Oral biofilms represent one of the most common niches for Candida biofilm formation (Douglas, 2002). Rats have predominantly been utilized to study host-biofilm interactions, particularly for the analysis of dental devices and the associated denture stomatitis (Nett et al, 2010;Lee et al, 2011;Johnson et al, 2012;Tobouti et al, 2016;Sultan et al, 2019;Yano et al, 2019). In these models, Candida spp.…”

Section: Insight Into Host Responses To Biofilm Through Animal Modelsmentioning

confidence: 99%

How Biofilm Growth Affects Candida-Host Interactions

Eix

Nett

2020

Front. Microbiol.

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Candida spp. proliferate as surface-associated biofilms in a variety of clinical niches. These biofilms can be extremely difficult to eradicate in healthcare settings. Cells within biofilm communities grow as aggregates and produce a protective extracellular matrix, properties that impact the ability of the host to respond to infection. Cells that disperse from biofilms display a phenotype of enhanced pathogenicity. In this review, we highlight host-biofilm interactions for Candida, focusing on how biofilm formation influences innate immune responses.

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Expression of Secreted Aspartyl Proteinases in an Experimental Model of Candida albicans‐Associated Denture Stomatitis

Cited by 25 publications

References 41 publications

Candida albicans Pathogenesis: Fitting within the Host-Microbe Damage Response Framework

Candida albicans Pathogenesis: Fitting within the Host-Microbe Damage Response Framework

Oral Candidiasis: A Disease of Opportunity

How Biofilm Growth Affects Candida-Host Interactions

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