Aspergillus fumigatus is one of the most prevalent pathogenic fungi. Its conidia are common in the environment and are naturally inhaled into the lung, but are promptly removed by host innate immunity. In host cells, A. fumigatus has been shown to trigger the activation of NF-954;B, but other transcription factors are also activated following the infection by this organism. We have reported that activation protein (AP)-1, a group of the host transcription factors that plays an important role in the production of cytokine and chemokine, is activated in dendritic cells during the infection by A. fumigatus. Swollen conidia but not resting conidia strongly induced the activation of AP-1 and were stained well with anti-1,3-β -glucan antibody, which suggests that the activation is related to β -glucan exposed on the surface of swollen conidia. Dectin-l is a well-known host receptor to recognize 1,3-β -glucan. When the HEK293T cells with exogenous dectin-I expression were treated by resting conidia or swollen conidia, the activation of AP-1 was induced only by swollen conidia. This suggests that the AP-l activation is induced via dectin-I through the recognition of 1,3-β -glucan. The activation of AP-1 was inhibited by the overexpression of dominant-negative form of Syk protein kinase, which is indicative that the activation of AP-l depends on the activity of Syk kinase. In this talk, I will present an overview of our data collected from in vitro experiments for further understanding of the innate immune system against aspergillosis.
Full conference title:
17th International Society for Human and Animal Mycology
- ISHAM 17th (2009)