| Summary: | <i>Aspergillus fumigatus</i> is a ubiquitous opportunistic pathogen. We have previously reported that volatile organic compounds (VOCs) produced by <i>A. fumigatus</i> cause delays in metamorphosis, morphological abnormalities, and death in a <i>Drosophila melanogaster</i> eclosion model. Here, we developed <i>A</i>. <i>fumigatus</i> deletion mutants with blocked oxylipin biosynthesis pathways (∆<i>ppoABC</i>) and then exposed the third instar larvae of <i>D. melanogaster</i> to a shared atmosphere with either <i>A. fumigatus</i> wild-type or oxylipin mutant cultures for 15 days. Fly larvae exposed to VOCs from wild-type <i>A</i>. <i>fumigatus</i> strains exhibited delays in metamorphosis and toxicity, while larvae exposed to VOCs from the ∆<i>ppoABC</i> mutant displayed fewer morphogenic delays and higher eclosion rates than the controls. In general, when fungi were pre-grown at 37 °C, the effects of the VOCs they produced were more pronounced than when they were pre-grown at 25 °C. GC–MS analysis revealed that the wild-type <i>A. fumigatus</i> Af293 produced more abundant VOCs at higher concentrations than the oxylipin-deficient strain Af293∆<i>ppoABC</i> did. The major VOCs detected from wild-type Af293 and its triple mutant included isopentyl alcohol, isobutyl alcohol, 2-methylbutanal, acetoin, and 1-octen-3-ol. Unexpectedly, compared to wild-type flies, the eclosion tests yielded far fewer differences in metamorphosis or viability when flies with immune-deficient genotypes were exposed to VOCs from either wild-type or ∆<i>ppoABC</i> oxylipin mutants. In particular, the toxigenic effects of <i>Aspergillus</i> VOCs were not observed in mutant flies deficient in the Toll (<i>spz<sup>6</sup></i>) pathway. These data indicate that the innate immune system of <i>Drosophila</i> mediates the toxicity of fungal volatiles, especially via the Toll pathway.
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