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We deeply phenotyped the lipidomic response to SARs\u2010CoV\u20102 and compared that with infection with other pathogens in patients admitted with acute respiratory distress syndrome to an intensive care unit (ICU).<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Mass spectrometry was used to characterise lipids and relate them to proteins, peripheral cell immunotypes and disease severity.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Circulating phospholipases (sPLA2, cPLA2 (PLA2G4A) and PLA2G2D) were elevated on admission in all ICU groups. Cyclooxygenase, lipoxygenase and epoxygenase products of arachidonic acid (AA) were elevated in all ICU groups compared with controls. sPLA2 predicted severity in COVID\u201019 and correlated with TxA2, LTE4 and the isoprostane, iPF2\u03b1\u2010III, while PLA2G2D correlated with LTE4. The elevation in PGD2, like PGI2 and 12\u2010HETE, exhibited relative specificity for COVID\u201019 and correlated with sPLA2 and the interleukin\u201013 receptor to drive lymphopenia, a marker of disease severity. Pro\u2010inflammatory eicosanoids remained correlated with severity in COVID\u201019 28 days after admission. Amongst non\u2010COVID ICU patients, elevations in 5\u2010 and 15\u2010HETE and 9\u2010 and 13\u2010HODE reflected viral rather than bacterial disease. Linoleic acid (LA) binds directly to SARS\u2010CoV\u20102 and both LA and its di\u2010HOME products reflected disease severity in COVID\u201019. In healthy marines, these lipids rose with seroconversion. Eicosanoids linked variably to the peripheral cellular immune response. PGE2, TxA2 and LTE4 correlated with T cell activation, as did PGD2 with non\u2010B non\u2010T cell activation. In COVID\u201019, LPS stimulated peripheral blood mononuclear cell PGF2\u03b1 correlated with memory T cells, dendritic and NK cells while LA and DiHOMEs correlated with exhausted T cells. Three high abundance lipids \u2013 ChoE 18:3, LPC\u2010O\u201016:0 and PC\u2010O\u201030:0 \u2013 were altered specifically in COVID. LPC\u2010O\u201016:0 was strongly correlated with T helper follicular cell activation and all three negatively correlated with multi\u2010omic inflammatory pathways and disease severity.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>A broad based lipidomic storm is a predictor of poor prognosis in ARDS. Alterations in sPLA2, PGD2 and 12\u2010HETE and the high abundance lipids, ChoE 18:3, LPC\u2010O\u201016:0 and PC\u2010O\u201030:0 exhibit relative specificity for COVID\u201019 amongst such patients and correlate with the inflammatory response to link to disease severity.<\/jats:p><\/jats:sec>","DOI":"10.1002\/ctm2.1440","type":"journal-article","created":{"date-parts":[[2023,11,10]],"date-time":"2023-11-10T18:20:32Z","timestamp":1699640432000},"source":"Crossref","is-referenced-by-count":40,"title":["Deep phenotyping of the lipidomic response in COVID\u201019 and non\u2010COVID\u201019 sepsis"],"prefix":"10.1002","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2224-5431","authenticated-orcid":false,"given":"Hu","family":"Meng","sequence":"first","affiliation":[{"name":"Institute for Translational Medicine and Therapeutics Perelman School of Medicine University of Pennsylvania  Philadelphia Pennsylvania 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