Siglecf Deficiency Prevents Fibrosis After Bleomycin-Induced Acute Lung Injury
Airway macrophages (AMs) are critical for resolving inflammation and repairing injured lung tissue, but can also contribute to the development of fibrosis.  AMs were isolated from bronchoalveolar lavage fluid of Siglec-F KO and WT mice prior to and 7, 14, and 21 days after bleomycin challenge (single dose, 2.5 units/kg, IT).  RNA was isolated using the Qiagen micro plus RNA kit and 200 ng of total RNA was used to generate RNA-Seq libraries.  The libraries were run on the NovaSeq 6000 with 80 million pair-end reads per sample. Overall design: To investigate the role of Siglec-F signaling in airspace macrophages (AMs) and contributions to development of fibrosis, we challenged mice with bleomycin (2.5 units/kg, IT) or saline vehicle.  We performed bulk RNAseq on AMs collected from wild type and Siglec-F deficient mice on days 7, 14, and 21 after bleo exposure to evaluate differentially expressed genes.