Publications by authors named "Kayleigh Earle"
Article Synopsis
- Aspergillus fumigatus causes the infection known as aspergillosis and uses asexual spores to infect hosts, but little is known about how it evades the immune system.
- In this study, researchers analyzed the conidial surface proteins of A. fumigatus and compared them to two non-pathogenic species, discovering 62 proteins unique to A. fumigatus.
- Testing null mutants for 42 genes revealed that deleting 33 of these genes affected the fungus's ability to resist immune responses, particularly highlighting a gene that influences the proinflammatory cytokine IL-1β, which is crucial for infection in a mouse model.
, an important pulmonary fungal pathogen causing several diseases collectively called aspergillosis, relies on asexual spores (conidia) for initiating host infection. Here, we used a phylogenomic approach to compare proteins in the conidial surface of , two closely related non-pathogenic species, and , and the cryptic pathogen . After identifying 62 proteins uniquely expressed on the conidial surface, we assessed null mutants for 42 genes encoding conidial proteins.
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- The study investigates the role of conidial surface proteins in the pathogenic fungus responsible for aspergillosis and compares it with non-pathogenic species.
- Researchers identified 62 proteins specifically expressed on the surface of the conidia and deleted genes for 42 of these proteins to assess their impact on infection.
- Findings indicate that certain proteins, particularly one related to IL-1β production, are crucial for the fungus in evading the immune response during initial host infection.
Pulmonary infections caused by the mould pathogen are a major cause of morbidity and mortality globally. Compromised lung defences arising from immunosuppression, chronic respiratory conditions or more recently, concomitant viral or bacterial pulmonary infections are recognised risks factors for the development of pulmonary aspergillosis. In this review, we will summarise our current knowledge of the mechanistic basis of pulmonary aspergillosis with a focus on emerging at-risk populations.
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