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Neutrophils, monocytes, and macrophages recruited to pathogen-infected lungs, including SARS-CoV-2\u2013infected lungs, express phosphatidylinositol 3-kinase gamma (PI3K\u03b3), a signaling protein that coordinates both granulocyte and monocyte trafficking to diseased tissues and immune-suppressive, profibrotic transcription in myeloid cells. PI3K\u03b3 deletion and inhibition with the clinical PI3K\u03b3 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\u03b3 in inflammatory lung disease and support the potential use of PI3K\u03b3 inhibitors to suppress inflammation in severe infectious diseases.\n                  <\/jats:p>","DOI":"10.1126\/scitranslmed.adi6887","type":"journal-article","created":{"date-parts":[[2024,7,3]],"date-time":"2024-07-03T13:59:54Z","timestamp":1720015194000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":13,"title":["PI3K\u03b3 inhibition circumvents inflammation and vascular leak in SARS-CoV-2 and other infections"],"prefix":"10.1126","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7488-369X","authenticated-orcid":true,"given":"Ryan M.","family":"Shepard","sequence":"first","affiliation":[{"name":"Moores Cancer Center, University of California, San Diego, La Jolla, CA 92093, 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