GSE119956
Transcriptome analysis of wild-type and Csf2-/- bone marrow-derived macrophages during legionella pneumophila infection
Pathogens have evolved a wide range of strategies to allow survival and subsequently cause diseases in human, however, it's still poorly understood how the immune system operates successfully to overcome pathogen-induced disturbance and enable robust immune responses against infection. The intracellular bacteria Legionella pneumophila has the ability to block host translation which causes global protein synthesis blockade in the target cells, but the host can still strongly evoke innate immune responses. We previously found that IL-1 signaling was critical for innate immunity during Legionella infection. Here, we further clarify that IL-1 signaling acts directly on alveolar epithelial cells, which potently drives granulocyte-macrophage colony-stimulating factor (GM-CSF) production by these cells, and importantly, GM-CSF signaling fundamentally promotes inflammatory immune responses in myeloid cells through cell-intrinsic transcriptional regulation via JAK2/STAT5 pathway. Our findings reveal that lung epithelial cells act as a key intermediator to facilitate communication between infected cells and bystander cells which is essential for antimicrobial defense. Overall design: Comparison of mRNA profiles between WT and Csf2-/- BMDMs with or without legionella pneumophila LP02flaA infection at 12 h by RNA sequencing analysis (two genotypes and two treatments in triplicate, a total of 12 samples)