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Aspergillus fumigatus conidial surface-associated proteome reveals factors for fungal evasion and host immunity modulation.
Pinzan, Camila Figueiredo; Valero, Clara; de Castro, Patrícia Alves; da Silva, Jefferson Luiz; Earle, Kayleigh; Liu, Hong; Horta, Maria Augusta Crivelente; Kniemeyer, Olaf; Krüger, Thomas; Pschibul, Annica; Cömert, Derya Nur; Heinekamp, Thorsten; Brakhage, Axel A; Steenwyk, Jacob L; Mead, Matthew E; Hermsdorf, Nico; Filler, Scott G; da Rosa-Garzon, Nathalia Gonsales; Delbaje, Endrews; Bromley, Michael J; Cabral, Hamilton; Diehl, Camila; Angeli, Claudia B; Palmisano, Giuseppe; Ibrahim, Ashraf S; Rinker, David C; Sauters, Thomas J C; Steffen, Karin; Gumilang, Adiyantara; Rokas, Antonis; Gago, Sara; Dos Reis, Thaila F; Goldman, Gustavo H.
Affiliation
  • Pinzan CF; Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, Brazil.
  • Valero C; Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, Brazil.
  • de Castro PA; Manchester Fungal Infection Group, Division of Evolution, Infection, and Genomics, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, UK.
  • da Silva JL; Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, Brazil.
  • Earle K; Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, Brazil.
  • Liu H; Manchester Fungal Infection Group, Division of Evolution, Infection, and Genomics, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, UK.
  • Horta MAC; Division of Infectious Diseases, Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, CA, USA.
  • Kniemeyer O; Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, Brazil.
  • Krüger T; Department of Molecular and Applied Microbiology, Leibniz Institute for Natural Product Research and Infection Biology (Leibniz-HKI) and Institute of Microbiology, Friedrich Schiller University, Jena, Germany.
  • Pschibul A; Department of Molecular and Applied Microbiology, Leibniz Institute for Natural Product Research and Infection Biology (Leibniz-HKI) and Institute of Microbiology, Friedrich Schiller University, Jena, Germany.
  • Cömert DN; Department of Molecular and Applied Microbiology, Leibniz Institute for Natural Product Research and Infection Biology (Leibniz-HKI) and Institute of Microbiology, Friedrich Schiller University, Jena, Germany.
  • Heinekamp T; Department of Molecular and Applied Microbiology, Leibniz Institute for Natural Product Research and Infection Biology (Leibniz-HKI) and Institute of Microbiology, Friedrich Schiller University, Jena, Germany.
  • Brakhage AA; Department of Molecular and Applied Microbiology, Leibniz Institute for Natural Product Research and Infection Biology (Leibniz-HKI) and Institute of Microbiology, Friedrich Schiller University, Jena, Germany.
  • Steenwyk JL; Department of Molecular and Applied Microbiology, Leibniz Institute for Natural Product Research and Infection Biology (Leibniz-HKI) and Institute of Microbiology, Friedrich Schiller University, Jena, Germany.
  • Mead ME; Howards Hughes Medical Institute and the Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA, USA.
  • Hermsdorf N; Department of Biological Sciences and Evolutionary Studies Initiative, Vanderbilt University, Nashville, TN, USA.
  • Filler SG; Department of Molecular and Applied Microbiology, Leibniz Institute for Natural Product Research and Infection Biology (Leibniz-HKI) and Institute of Microbiology, Friedrich Schiller University, Jena, Germany.
  • da Rosa-Garzon NG; Division of Infectious Diseases, Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, CA, USA.
  • Delbaje E; David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
  • Bromley MJ; Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, Brazil.
  • Cabral H; Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, Brazil.
  • Diehl C; Manchester Fungal Infection Group, Division of Evolution, Infection, and Genomics, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, UK.
  • Angeli CB; Antimicrobial Resistance Network, University of Manchester, Manchester, UK.
  • Palmisano G; Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, Brazil.
  • Ibrahim AS; Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, Brazil.
  • Rinker DC; Departamento de Parasitologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil.
  • Sauters TJC; Departamento de Parasitologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil.
  • Steffen K; Division of Infectious Diseases, Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, CA, USA.
  • Gumilang A; David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
  • Rokas A; Department of Biological Sciences and Evolutionary Studies Initiative, Vanderbilt University, Nashville, TN, USA.
  • Gago S; Department of Biological Sciences and Evolutionary Studies Initiative, Vanderbilt University, Nashville, TN, USA.
  • Dos Reis TF; Department of Biological Sciences and Evolutionary Studies Initiative, Vanderbilt University, Nashville, TN, USA.
  • Goldman GH; Department of Biological Sciences and Evolutionary Studies Initiative, Vanderbilt University, Nashville, TN, USA.
Nat Microbiol ; 9(10): 2710-2726, 2024 Oct.
Article in En | MEDLINE | ID: mdl-39191887
ABSTRACT
Aspergillus fumigatus causes aspergillosis and relies on asexual spores (conidia) for initiating host infection. There is scarce information about A. fumigatus proteins involved in fungal evasion and host immunity modulation. Here we analysed the conidial surface proteome of A. fumigatus, two closely related non-pathogenic species, Aspergillus fischeri and Aspergillus oerlinghausenensis, as well as pathogenic Aspergillus lentulus, to identify such proteins. After identifying 62 proteins exclusively detected on the A. fumigatus conidial surface, we assessed null mutants for 42 genes encoding these proteins. Deletion of 33 of these genes altered susceptibility to macrophage, epithelial cells and cytokine production. Notably, a gene that encodes a putative glycosylasparaginase, modulating levels of the host proinflammatory cytokine IL-1ß, is important for infection in an immunocompetent murine model of fungal disease. These results suggest that A. fumigatus conidial surface proteins are important for evasion and modulation of the immune response at the onset of fungal infection.
Subject(s)

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Aspergillosis / Aspergillus fumigatus / Spores, Fungal / Fungal Proteins / Proteome / Immune Evasion Limits: Animals / Female / Humans Language: En Journal: Nat Microbiol Year: 2024 Type: Article Affiliation country: Brazil

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Aspergillosis / Aspergillus fumigatus / Spores, Fungal / Fungal Proteins / Proteome / Immune Evasion Limits: Animals / Female / Humans Language: En Journal: Nat Microbiol Year: 2024 Type: Article Affiliation country: Brazil