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The immune mechanisms that recognize inhaled  Aspergillus fumigatus  conidia to promote their elimination from the lungs are incompletely understood. FleA is a lectin expressed by  Aspergillus fumigatus  that has twelve binding sites for fucosylated structures that are abundant in the glycan coats of multiple plant and animal proteins. The role of FleA is unknown: it could bind fucose in decomposed plant matter to allow  Aspergillus fumigatus  to thrive in soil, or it may be a virulence factor that binds fucose in lung glycoproteins to cause  Aspergillus fumigatus  pneumonia. Our studies show that FleA protein and  Aspergillus fumigatus  conidia bind avidly to purified lung mucin glycoproteins in a fucose-dependent manner. In addition, FleA binds strongly to macrophage cell surface proteins, and macrophages bind and phagocytose  fleA- deficient  (∆fleA ) conidia much less efficiently than wild type (WT) conidia. Furthermore, a potent fucopyranoside glycomimetic inhibitor of FleA inhibits binding and phagocytosis of WT conidia by macrophages, confirming the specific role of fucose binding in macrophage recognition of WT conidia. Finally, mice infected with  ΔfleA  conidia had more severe pneumonia and invasive aspergillosis than mice infected with WT conidia. These findings demonstrate that FleA is not a virulence factor for  Aspergillus fumigatus . Instead, host recognition of FleA is a critical step in mechanisms of mucin binding, mucociliary clearance, and macrophage killing that prevent  Aspergillus fumigatus  pneumonia.

FleA Expression in Aspergillus fumigatus Is Recognized by Fucosylated Structures on Mucins and Macrophages to Prevent Lung Infection