ATAC-seq in wild type and EGR2 knock-out mouse alveolar macrophages

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: ATAC-seq in wild type and EGR2 knock-out mouse alveolar macrophages were performed from C57BL6 background control and EGR2 myeloid-specific conditional knock-out mice. The mice were euthanized by isoflurane inhalation then we isolated the cells from bronchoalveolar lavage. We sorted the CD45+ and F4/80+ alveolar macrophages. We did not apply any treatment.