Friendly fungi: symbiosis with commensal Candida albicans

Candida species are the most prevalent cause of invasive fungal infections, of which Candida albicans is the most common. Translocation across the epithelial barrier into the bloodstream by intestinal-colonizing C. albicans cells serves as the main source for systemic infections. Understanding the fungal mechanisms behind this process will give valuable insights on how to prevent such infections and keep C. albicans in the commensal state in patients with predisposing conditions. This review will focus on recent developments in characterizing fungal translocation mechanisms, compare what we know about enteric bacterial pathogens with C. albicans , and discuss the different proposed hypotheses for how C. albicans enters and disseminates through the bloodstream immediately following translocation.

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“… 34 , 35 The role that these adaptive immune responses play in colonization and infection of C. albicans has been recently reviewed. 36 , 37 …”

Section: Intestinal Colonization Phenotypementioning

confidence: 99%

From intestinal colonization to systemic infections: Candida albicans translocation and dissemination

2022

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“…Hyphae are also the main target of secreted IgA produced in response to C. albicans intestinal colonization, and the competitive fitness of C. albicans negatively correlates with the filamentation potential [ 106 ••, 113 , 117 ••, 118 ••]. In addition to antibody production, GI tract colonization with C. albicans induces robust Th17 responses, which reduce susceptibility to systemic candidiasis and disseminated infection with extracellular bacteria (reviewed in [ 119 ]) (Fig. 3 A).…”

Section: Colonization Of the Gut: A Source For Disseminated Infectionmentioning

confidence: 99%

“…3 A). While these responses can aggravate inflammatory conditions such as asthma or colitis, the beneficial effects of colonization-induced immunological changes might dominate for most individuals [ 119 ]. Interestingly, priming of systemic Th17 immunity by C. albicans colonization requires dynamic fluctuation of the expression of UME6 , which is a transcriptional regulator of filamentation, and exposure of the immunogenic cell wall moieties mannan and β-glucan [ 120 ••].…”

Section: Colonization Of the Gut: A Source For Disseminated Infectionmentioning

confidence: 99%

The Role of Host and Fungal Factors in the Commensal-to-Pathogen Transition of Candida albicans

Jacobsen

2023

Curr Clin Micro Rpt

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Purpose of Review The fungus Candida albicans has evolved to live in close association with warm-blooded hosts and is found frequently on mucosal surfaces of healthy humans. As an opportunistic pathogen, C. albicans can also cause mucosal and disseminated infections (candidiasis). This review describes the features that differentiate the fungus in the commensal versus pathogenic state and the main factors underlying C. albicans commensal-to-pathogen transition. Recent Findings Adhesion, invasion, and tissue damage are critical steps in the infection process. Especially invasion and damage require transcriptional and morphological changes that differentiate C. albicans in the pathogenic from the commensal state. While the commensal-to-pathogen transition has some conserved causes and features in the oral cavity, the female urogenital tract, and the gut, site-specific differences have been identified in recent years. Summary This review highlights how specific factors in the different mucosal niches affect development of candidiasis. Recent evidence suggests that colonization of the gut is not only a risk factor for systemic candidiasis but might also provide beneficial effects to the host.

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“…IL-34 is able to promote the conversion of M1 to M2, which may benefit the skin in establishing immune tolerance and wound healing (Diez-Orejas et al, 2018b). C. albicans can inhibit host inflammatory responses in the skin mucosa by inhibiting LPSinduced IL-12p70 production, while lower IL-12p70 production can avoid unnecessary Th1 responses to maintain immune tolerance, which may be one of the mechanisms by which 10.3389/fmicb.2022.1029966 C. albicans achieves a successful symbiotic lifestyle without compromising host health (Shao et al, 2022). IL-12p70 is an important proinflammatory cytokine that determines Th1 polarization, inhibits LPS-induced IL-12p70 production, and may be a key mechanism of C. albicans-induced immune tolerance.…”

Section: Candida Albicans Mediates Macrophages Immune Tolerancementioning

confidence: 99%

The advances in the regulation of immune microenvironment by Candida albicans and macrophage cross-talk

Zhao

Shang²,

Guo³

et al. 2022

Front. Microbiol.

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Candida albicans (C. albicans) is the most common causative agent of invasive fungal infections in hospitals. The body defends against and eliminates C. albicans infection by various mechanisms of immune response, and the latter mechanism of immune evasion is a major challenge in the clinical management of C. albicans infection. The role of macrophages in combating C. albicans infection has only recently been recognized, but the mechanisms remain to be elucidated. This review focuses on the interaction between C. albicans and macrophages (macrophages), which causes the body to generate an immune response or C. albicans immune escape, and then regulates the body’s immune microenvironment, to explore the effect of C. albicans virulence resistance vs. macrophage killing and clarify the role and mechanism of C. albicans pathogenesis. In general, a thorough understanding of the molecular principles driving antifungal drug resistance is essential for the development of innovative treatments that can counteract both existing and emerging fungal threats.

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Friendly fungi: symbiosis with commensal Candida albicans

Cited by 22 publications

References 102 publications

From intestinal colonization to systemic infections: Candida albicans translocation and dissemination

From intestinal colonization to systemic infections: Candida albicans translocation and dissemination

The Role of Host and Fungal Factors in the Commensal-to-Pathogen Transition of Candida albicans

The advances in the regulation of immune microenvironment by Candida albicans and macrophage cross-talk

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