Abstract
Airborne opportunistic fungi, including Aspergillus and other less common saprophytic molds, have recently emerged as important causes of mortality in immunocompromised individuals. Understanding the molecular mechanisms of host-fungal interplay in robust experimental pathosystems is becoming a research priority for development of novel therapeutics to combat these devastating infections. Over the past decade, invertebrate hosts with evolutionarily conserved innate immune signaling pathways and powerful genetics, such as Drosophila melanogaster, have been employed as a means to overcome logistic restrains associated with the use mammalian models of fungal infections. Recent studies in Drosophila models of filamentous fungi demonstrated that several genes implicated in fungal virulence in mammals also play a similarly important pathogenic role in fruit flies, and important host-related aspects in fungal pathogenesis are evolutionarily conserved. In view of recent advances in Drosophila genetics, fruit flies will become an invaluable surrogate model to study immunopathogenesis of fungal diseases.
Highlights
In recent years, opportunistic fungi have emerged as leading causes of morbidity and mortality in immunocompromised individuals [1,2,3]
Pioneering studies over the past decade demonstrated that a variety of opportunistic fungi can invade and cause fatal infection in a variety of simple invertebrate hosts, such as the fruit fly Drosophila melanogaster, and the roundworm Caenorhabditis elegans [13,14,15,16,17,18,19,20]
The alb1 Aspergillus fumigatus mutant, which is hypovirulent in mice, exhibited attenuated virulence in Toll-deficient flies only when introduced by feeding or rolling [20]
Summary
Opportunistic fungi have emerged as leading causes of morbidity and mortality in immunocompromised individuals [1,2,3]. Pioneering studies over the past decade demonstrated that a variety of opportunistic fungi can invade and cause fatal infection in a variety of simple invertebrate hosts, such as the fruit fly Drosophila melanogaster, and the roundworm Caenorhabditis elegans [13,14,15,16,17,18,19,20]. It has become evident from these studies that important aspects of innate immunity have been evolutionarily conserved across phylogeny. Parallel to GNBP3, a second detection system senses the activity of proteolytic virulence factors that are released in the fly hemolymph during invasive fungal growth and redundantly activates Toll pathway via the protease Persephone [27]
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