Project description:To investigate transcriptomic differences using RNA-seq in macrophages from a BM origin (CD45.1) and embryonic origin (CD45.2) in influenza-experienced, and naive lungs - at baseline and following stimulation
Project description:To investigate differences in the chromatin accessibility using ATAC-seq. This was done in macrophages from a BM origin (CD45.1) and embryonic origin (CD45.2) in influenza-experienced, and naive lungs - at baseline and following Pam3CSK4 stimulation
Project description:To investigate transcriptomic differences using RNA-seq. This was done in macrophages isolated from a busulfan chimera, using congenic markers (CD45.1 for a BM origin, and CD45.2 for a host origin) in influenza-experienced, and naive lungs - at baseline and following Pam3CSK4 stimulation
Project description:To investigate differences in the chromatin accessibility using ATAC-seq. This was done in macrophages isolated from a busulfan chimera, using congenic markers (CD45.1 for a BM origin, and CD45.2 for a host origin) in influenza-experienced, and naive lungs - at baseline and following Pam3CSK4 stimulation
Project description:Despite the prevalence and clinical importance of influenza, its long-term effect on lung immunity is unclear. Here we describe that following viral clearance and clinical recovery, at 1 month after infection with influenza, mice are better protected from Streptococcus pneumoniae infection due to a population of monocyte-derived alveolar macrophages (AMs) that produce increased interleukin-6. Influenza-induced monocyte-derived AMs have a surface phenotype similar to resident AMs but display a unique functional, transcriptional and epigenetic profile that is distinct from resident AMs. In contrast, influenza-experienced resident AMs remain largely similar to naive AMs. Thus, influenza changes the composition of the AM population to provide prolonged antibacterial protection. Monocyte-derived AMs persist over time but lose their protective profile. Our results help to understand how transient respiratory infections, a common occurrence in human life, can constantly alter lung immunity by contributing monocyte-derived, recruited cells to the AM population.
