Invasive pulmonary aspergillosis is acquired through inhalation of conidia. Little is known about early interactions between Aspergillus fumigatus conidia and alveolar epithelial cells, so an in vitro model was developed to study binding between conidia and A549 cells, a line of type II pneumocytes. Conidia rapidly became attached to confluent monolayers of A549 cells in serum-free medium, reaching a plateau within 40 min. Scanning electron microscopy (EM) showed a random pattern of early adherence; viable conidia subsequently became clustered on pneumocyte surfaces. Following germination of pneumocyte-adherent conidia for 12 h, direct penetration of epithelial cells by hyphae could be demonstrated by scanning and transmission EM. These data suggest that an early event following inhalation of A. fumigatus conidia may be binding of conidia to pneumocytes, followed by hyphal penetration of the epithelial cell layer.

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Aspergillus fumigatus has previously been shown to produce a soluble extracellular inhibitor of the alternative complement pathway, called Aspergillus complement inhibitor, or CI. We now report an efficient method for production of CI which relies on the fact that poorly conidiating cultures yielded CI activity with approximately sevenfold-higher potency than CI produced by conidiating cultures. CI from poorly conidiating cultures provided 50% inhibition of alternative pathway-mediated binding of '25I-labeled complement component C3 to cryptococcal blastoconidia at a mean concentration of 60 ,ug/ml. The ability of crude CI to 3508