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Invasive aspergillosis (IA) is a life-threatening disease that occurs in immunodepressed patients when infected with  Aspergillus fumigatus . This fungus is the second most-common causative agent of fungal disease after  Candida albicans . Nevertheless, much remains to be learned about the mechanisms by which  A. fulmigatus  activates the innate immune system. We investigated the inflammatory response to conidia and hyphae of  A. fumigatus  and specifically, their capacity to trigger activation of an inflammasome. Our results show that in contrast to conidia, hyphal fragments induce NLRP3 inflammasome assembly, caspase-1 activation and IL-1β release from a human monocyte cell line. The ability of  Aspergillus  hyphae to activate the NLRP3 inflammasome in the monocytes requires K +  efflux and ROS production. In addition, our data show that NLRP3 inflammasome activation as well as pro-IL-1β expression relies on the Syk tyrosine kinase, which is downstream from the pathogen recognition receptor Dectin-1, reinforcing the importance of Dectin-1 in the innate immune response against fungal infection. Furthermore, we show that treatment of monocytes with corticosteroids inhibits transcription of the gene encoding IL-1β. Thus, our data demonstrate that the innate immune response against  A. fumigatus  infection involves a two step activation process, with a first signal promoting expression and synthesis of pro-IL-1β; and a second signal, involving Syk-induced activation of the NLRP3 inflammasome and caspase-1, allowing processing and secretion of the mature cytokine.

Aspergillus fumigatus Stimulates the NLRP3 Inflammasome through a Pathway Requiring ROS Production and the Syk Tyrosine Kinase