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Published on: March 22, 2024
Psoriasin, a novel anti-Candida albicans adhesin
Annelie Brauner1, Cathrin Alvendal2, Milan Chromek3
1Department of Microbiology, Tumor and Cell Biology, Division of Clinical Microbiology, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden. Annelie.Brauner@ki.se.
Abstract:
Candida albicans belongs to the normal microbial flora on epithelial surfaces of humans. However, under certain, still not fully understood conditions, it can become pathogenic and cause a spectrum of diseases, from local infections to life-threatening septicemia. We investigated a panel of antimicrobial proteins and peptides (AMPs), potentially involved in mucosal immunity against this pathogen. Out of six studied AMPs, psoriasin was most up-regulated during a mucosal infection, an acute episode of recurrent Candida vulvovaginitis, although candidacidal activity has not been demonstrated. We here show that psoriasin binds to β-glucan, a basic component of the C. albicans cell wall, and thereby inhibits adhesion of the pathogen to surfaces and increases IL-8 production by mucosal epithelial cells. In conclusion, we show a novel mechanism of action of psoriasin. By inhibiting C. albicans adhesion and by enhancing cytokine production, psoriasin contributes to the immune response against C. albicans. KEY MESSAGES: The antimicrobial peptide psoriasin is highly up-regulated during a local mucosal infection, Candida albicans vulvovaginitis. Psoriasin binds to β-glucan in the Candida albicans cell wall and thereby inhibits adhesion of the pathogen. Binding of psoriasin to Candida albicans induces an immune response by mucosal epithelial cells.
Insights
Psoriasin, an antimicrobial peptide, combats Candida albicans by blocking pathogen adhesion to surfaces. This binding also stimulates an immune response from epithelial cells, aiding mucosal immunity.
Area of Science:
- Immunology
- Microbiology
- Biochemistry
Background:
- Candida albicans is a common human commensal that can become pathogenic, causing infections from localized disease to sepsis.
- Mucosal immunity plays a critical role in controlling Candida albicans, involving antimicrobial proteins and peptides (AMPs).
- Psoriasin is an AMP identified as highly upregulated during Candida albicans vulvovaginitis, but its direct candidacidal activity was unknown.
Purpose of the Study:
- To investigate the mechanism of action of psoriasin against Candida albicans.
- To determine if psoriasin plays a role in mucosal immunity against Candida albicans.
- To elucidate how psoriasin interacts with Candida albicans and influences the host immune response.
Main Methods:
- Investigated a panel of antimicrobial proteins and peptides (AMPs) for activity against Candida albicans.
- Assessed psoriasin upregulation during a mucosal infection model (Candida albicans vulvovaginitis).
- Examined psoriasin's binding to Candida albicans cell wall components, specifically β-glucan.
- Evaluated psoriasin's effect on Candida albicans adhesion to surfaces.
- Measured IL-8 production by mucosal epithelial cells upon interaction with psoriasin and Candida albicans.
Main Results:
- Psoriasin was significantly upregulated during acute Candida albicans vulvovaginitis.
- Psoriasin demonstrated binding to β-glucan, a key component of the Candida albicans cell wall.
- This binding inhibited the adhesion of Candida albicans to surfaces.
- Psoriasin binding to Candida albicans enhanced IL-8 production by mucosal epithelial cells, indicating an immune response.
Conclusions:
- Psoriasin exhibits a novel mechanism of action against Candida albicans by inhibiting pathogen adhesion.
- Psoriasin contributes to mucosal immunity by preventing Candida albicans colonization and by stimulating an inflammatory cytokine response.
- These findings highlight psoriasin's dual role in innate immunity against fungal pathogens.
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