The next IECB monthly seminar will be held on January 30th at 11am.

The speaker,  Prof.  Gustavo H. Goldman  from São Paulo University,  

will present a seminar entitled:  "Aspergillus fumigatus conidial surface-associated proteome reveals factors for fungal evasion and host immunity modulation".

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-1β, is important for infection in an immunocompetent murine model of fungal disease. We also characterized CyrA (a cysteine-rich protein), as a secreted protein important for the induction of pro-inflammatory cytokines and virulence in an immunocompetent murine model of fungal disease. A. fumigatus wild-type exposed to murine macrophages induces the production of eicosanoids/prostaglandins EPA2, PGE2, PGD2, and 15-oxo-ETE. The ΔcyrA mutant has increased levels of PGE2 and PGD2 suggesting CyrA is involved in their modulation. High CyrA-specific IgG responses were found in antisera from individual patients with invasive pulmonary aspergillosis, suggesting a role for CyrA in A. fumigatus pathogenesis. 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.