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Immune evasion by acquisition of complement inhibitors: the mould Aspergillus binds both factor H and C4b binding
1Department for Hygiene, Microbiology & Social Medicine, Innsbruck Medical University, Austria.
Abstract:
Pathogenic fungi represent a major threat particularly to immunocompromised hosts, leading to severe, and often lethal, systemic opportunistic infections. Although the impaired immune status of the host is clearly the most important factor leading to disease, virulence factors of the fungus also play a role. Factor H (FH) and its splice product FHL-1 represent the major fluid phase inhibitors of the alternative pathway of complement, whereas C4b-binding protein (C4bp) is the main fluid phase inhibitor of the classical and lectin pathways. Both proteins can bind to the surface of various human pathogens conveying resistance to complement destruction and thus contribute to their pathogenic potential. We have recently shown that Candida albicans evades complement by binding both Factor H and C4bp. Here we show that moulds such as Aspergillus spp. bind Factor H, the splicing variant FHL-1 and also C4bp. Immunofluorescence and flow cytometry studies show that the binding of Factor H and C4bp to Aspergillus spp. appears to be even stronger than to Candida spp. and that different, albeit possibly nearby, binding moieties mediate this surface attachment.
Insights
Pathogenic fungi like Aspergillus spp. evade the immune system by binding complement inhibitors Factor H (FH) and C4b-binding protein (C4bp). This fungal immune evasion is stronger in Aspergillus than Candida, contributing to opportunistic infections.
Area of Science:
- Medical Mycology
- Immunology
- Microbial Pathogenesis
Background:
- Pathogenic fungi cause severe opportunistic infections, especially in immunocompromised individuals.
- Fungal virulence factors contribute to disease, alongside host immune status.
- Complement system inhibitors like Factor H (FH), FHL-1, and C4b-binding protein (C4bp) protect against complement-mediated destruction.
Purpose of the Study:
- To investigate the binding of complement inhibitors FH, FHL-1, and C4bp to Aspergillus species.
- To compare the binding affinity of these inhibitors to Aspergillus spp. versus Candida albicans.
- To identify potential surface binding sites involved in fungal complement evasion.
Main Methods:
- Immunofluorescence microscopy to visualize binding of FH and C4bp.
- Flow cytometry to quantify the binding of FH, FHL-1, and C4bp.
- Comparative analysis of binding to Aspergillus spp. and Candida albicans.
Main Results:
- Aspergillus species were shown to bind FH, FHL-1, and C4bp.
- Binding of FH and C4bp to Aspergillus spp. was observed to be stronger than to Candida albicans.
- Evidence suggests distinct surface moieties mediate FH and C4bp binding on Aspergillus.
Conclusions:
- Aspergillus spp. utilize FH and C4bp for immune evasion by preventing complement-mediated killing.
- The enhanced binding of FH and C4bp to Aspergillus may contribute to their pathogenic potential.
- Understanding these fungal-host interactions is crucial for developing antifungal strategies.
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