Skin Immunity to Candida albicans

Treatment of patients with glucocorticoids can result in an increased risk of infection with pathogens such as fungi. Dectin-1 is a member of the C-type lectin receptor superfamily and was shown to be one of the major receptors for fungal beta-glucans. Activation of Dectin-1 increases the production of cytokines and chemokines and T-cell stimulatory capacity of DC and mediates resolution of fungal infections. Here we show that antigen-presenting cells generated in the presence of dexamethasone (Dex-DC) have a reduced capacity to stimulate T-cell proliferation and decreased expression of costimulatory molecules, that can not be enhanced upon stimulation with Dectin-1 ligands. Stimulation of Dex-DC with beta-glucans induced a strong upregulation of Syk phosphorylation and increased secretion of IL-10, while the production of IL-12, IL-23 and TNF-alpha was reduced. Downstream of Syk stimulation of Dectin-1 on Dex-DC resulted in phosphorylation of STAT3 and reduced nuclear localization of transcription factors involved in DC activation and function.

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“…Additionally IL-17 produced by Th17 cells is essential for initial recruitment of neutrophils to the site of infection 50 .…”

Section: Discussionmentioning

confidence: 99%

Dexamethasone induced inhibition of Dectin-1 activation of antigen presenting cells is mediated via STAT-3 and NF-κB signaling pathways

Kotthoff

Heine

Held

et al. 2017

Sci Rep

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“…Indeed, no infectious symptoms are generally observed in healthy persons. In individuals with weakened immunity, Candida yeasts can cause annoying and painful superficial infections, such as oral thrush, cutaneous candidiasis or candidal vulvovaginitis . In severely ill and immunocompromised persons, including hospitalized patients after surgical treatment, organ transplantation or anticancer therapy, disseminated, multi‐organ, and systemic candidiasis often develops and is associated with high morbidity and mortality …”

Section: Introductionmentioning

confidence: 99%

Extracellular proteinases of Candida species pathogenic yeasts

Rapała‐Kozik

Bocheńska

Zając

et al. 2018

Molecular Oral Microbiology

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The increased incidence of severe disseminated infections caused by the opportunistic yeast-like fungi Candida spp. highlights the urgent need for research into the major virulence factors of these pathogens-extracellular aspartic proteinases of the candidapepsin and yapsin families. Classically, these enzymes were considered to be generally destructive factors that damage host tissues and provide nutrients for pathogen propagation. However, in recent decades, novel and more specific functions have been suggested for extracellular candidal proteinases. These include contributions to cell wall maintenance and remodeling, the formation of polymicrobial biofilms, adhesion to external protective barriers of the host, the deregulation of host proteolytic cascades (such as the complement system, blood coagulation and the kallikrein-kinin system), a dysregulated host proteinase-inhibitor balance, the inactivation of host antimicrobial peptides, evasion of immune responses and the induction of inflammatory mediator release from host cells. Only a few of these activities recognized in Candida albicans candidapepsins have been also confirmed in other Candida species, and characterization of Candida glabrata yapsins remains limited.

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“…Candida albicans (C. albicans) is a yeast that naturally colonizes the skin, mucosa, gastrointestinal, and reproductive tract. 1 In addition to its communalistic relationship with the host, Candida is also known to be a major cause of opportunistic infections. Depending on the defect of the host's immune system, Candida infection can range from benign localized to systemic life-threatening.…”

Section: Introductionmentioning

confidence: 99%