ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR278/082/SRR27892082/SRR27892082_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR278/086/SRR27892086/SRR27892086_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR278/084/SRR27892084/SRR27892084_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR278/080/SRR27892080/SRR27892080_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR278/082/SRR27892082/SRR27892082_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR278/085/SRR27892085/SRR27892085_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR278/084/SRR27892084/SRR27892084_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR278/081/SRR27892081/SRR27892081_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR278/083/SRR27892083/SRR27892083_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR278/081/SRR27892081/SRR27892081_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR278/080/SRR27892080/SRR27892080_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR278/083/SRR27892083/SRR27892083_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR278/085/SRR27892085/SRR27892085_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR278/086/SRR27892086/SRR27892086_2.fastq.gzprimaryOK200GenomicsMoores Cancer Center, Pathology, University of California, San Diegohttps://www.ebi.ac.uk/ena/browser/view/PRJNA1073955Mus musculusVirulent infectious agents such as SARS-CoV-2 and Methicillin Resistant Staphylococcus Aureus (MRSA) induce tissue damage that recruits neutrophils and monocyte/macrophages, leading to T cell exhaustion, fibrosis, vascular leak, epithelial cell depletion, and fatal organ damage. Neutrophils, monocytes and macrophages recruited to pathogen-infected lungs, including SARS-CoV-2 infected lungs, express phosphatidylinositol 3-kinase gamma (PI3K a signaling protein that coordinately controls granulocyte and monocyte trafficking to diseased tissues and immune suppressive, pro-fibrotic transcription in myeloid cells. PI3K deletion and inhibition with the clinical PI3K inhibitor eganelisib promoted survival in models of infectious diseases, including SARS-CoV-2 and MRSA, by suppressing inflammation, vascular leak, organ damage and cytokine storm. These results demonstrate essential roles for PI3K in inflammatory lung disease and support the potential use of PI3K inhibitors to suppress inflammation in severe infectious diseases. Overall design: Human ACE2 transgenic mice were inoculated with SARS-CoV-2 and treated with the PI3Kgamma inhbitor IPI-549 or vehicle. Lungs of treated mice (4 IPI-549 and 3 Vehicle) were isolated three days later and stored in TRIZOL until RNA was isolated, and ribodepleted libaries were synthesized and sequenced.xref:PubMed:38959328ENAfalsePI3Kg inhibition circumvents inflammation and mortality in SARS-CoV-2 and other infectionsPI3Kg inhibition circumvents inflammation and mortality in SARS-CoV-2 and other infections2025-09-242024-03-30PRJNA1073955GSE2552111009038959328