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Non-canonical signalling mediates changes in fungal cell wall PAMPs that drive immune evasion
Arnab Pradhan1,2, Gabriela M Avelar1, Judith M Bain1
1Institute of Medical Sciences, Foresterhill, Aberdeen, UK.
Abstract:
To colonise their host, pathogens must counter local environmental and immunological challenges. Here, we reveal that the fungal pathogen Candida albicans exploits diverse host-associated signals to promote immune evasion by masking of a major pathogen-associated molecular pattern (PAMP), β-glucan. Certain nutrients, stresses and antifungal drugs trigger β-glucan masking, whereas other inputs, such as nitrogen sources and quorum sensing molecules, exert limited effects on this PAMP. In particular, iron limitation triggers substantial changes in the cell wall that reduce β-glucan exposure. This correlates with reduced phagocytosis by macrophages and attenuated cytokine responses by peripheral blood mononuclear cells. Iron limitation-induced β-glucan masking depends on parallel signalling via the iron transceptor Ftr1 and the iron-responsive transcription factor Sef1, and the protein kinase A pathway. Our data reveal that C. albicans exploits a diverse range of specific host signals to trigger protective anticipatory responses against impending phagocytic attack and promote host colonisation.
Insights
The fungus Candida albicans hides its immune-triggering beta-glucan (β-glucan) using host signals like iron limitation. This immune evasion helps the pathogen colonize its host.
Area of Science:
- Mycology
- Immunology
- Pathogen Biology
Background:
- Pathogens must overcome host defenses for colonization.
- Candida albicans is a major fungal pathogen.
- Immune evasion is crucial for pathogen survival.
Purpose of the Study:
- Investigate how Candida albicans evades the host immune system.
- Identify host-associated signals that trigger immune evasion mechanisms.
- Elucidate the molecular pathways involved in immune evasion.
Main Methods:
- Analysis of Candida albicans cell wall composition.
- Assays for phagocytosis by macrophages.
- Measurement of cytokine responses from peripheral blood mononuclear cells.
- Genetic analysis of signaling pathways (Ftr1, Sef1, Protein Kinase A).
Main Results:
- Candida albicans masks its beta-glucan (β-glucan) in response to host signals.
- Iron limitation significantly reduces β-glucan exposure.
- Reduced β-glucan exposure correlates with decreased phagocytosis and attenuated immune responses.
- Iron limitation-induced masking involves Ftr1, Sef1, and Protein Kinase A signaling.
Conclusions:
- Candida albicans utilizes host signals, particularly iron limitation, to mask β-glucan and evade immune detection.
- This adaptive strategy involves specific molecular signaling pathways.
- The findings reveal a mechanism for immune evasion that promotes fungal colonization.
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