c-Jun and CREB1 transcription factor binding analysis in wild type bone marrow-derived macrophages in response to type II interferon and stress

The innate immune system acts as the first line of defense against invasion of microbial pathogens. Here, macrophages play a substantial role in recognition, phagocytosis and killing of pathogens and the regulation of the innate immune response. Here, interferons play a crucial role in augmenting the antimicrobial functions of macrophages and their ability to produce mediators of immunoregulation. Pathogen recognition activates many different signaling pathways that interact to produce an innate response commensurate with the microbial challenge. The co-occurrence of signaling by sensors of stress and IFN receptors is a hallmark of innate responses to many viral and bacterial pathogens. Our results show c-Jun and CREB binding upon Anisomycin, a drug that induces stress-activation of MAPK pathways, IFNg stimulation and the combination of both or with p38 inhibitor PH-797804 and JNK inhibitor SP600125, Anisomycin and IFNg. Overall design: Methods: Bone marrow derived-macrophages (BMDM) chromatin of wild-type (WT) untreated, as well as 2h20 Anisomycin, 2h IFNg treated or pre-treated with Anisomycin (20min) and then stimulated with IFNg for for 2h or pre-treated with PH-797804 and SP600125 followed by pre-treatment with Anisomycin and stimulated with IFNg and then were generated by deep sequencing, in triplicate, using Illumina sequencing.