RNA-seq in wild type and EGR2 knock-out mouse alveolar macrophages upon vehicle and zymosan treatment

The alveolar macrophages (AMs) as a component of the innate immunity of the lung play important role in the elimination of inhaled microbes and harmful agents. The transcription factor EGR2 is a known marker transcription factor of AMs but its exact epigenetic and transcriptomic effects have not been examined. In our study, we performed ATAC-seq and RNA-seq in WT and EGR2 deficient alveolar macrophages to describe the mechanism of action and to predict potential direct target genes of EGR2. Clec7a is one of the targets of this transcription factor which is essential in the zymosan-induced inflammatory response. We further analyzed this process by applying in vivo mouse model. Our findings demonstrate that EGR2 is a key transcriptional activator, responsible for the intact protective program against different pathogens, especially fungi in AMs. Overall design: RNA-seq in wild-type and EGR2 knock-out mouse alveolar macrophages were performed upon vehicle control and zymosan treatment. The mice were intranasally treated with 300 µg zymosan in 40 µl PBS+2 mM NaN3 for 6 hours and 24 hours or just with 40 µl PBS+2 mM NaN3 as vehicle control. The mice were euthanized by isoflurane inhalation then the cellular components were isolated through bronchoalveolar lavage. We sorted the CD45+ and F4/80+ alveolar macrophages.