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PXD028429-1

PXD028429 is an original dataset announced via ProteomeXchange.

Dataset Summary
TitleProteomics of serum samples from COVID-19 ARDS and bacterial ARDS patients
DescriptionSARS-CoV-2 is a novel coronavirus that causes acute respiratory distress syndrome (ARDS), death and long-term sequelae. Innate immune cells are critical for host defense but are also the primary drivers of ARDS. The relationships between innate cellular responses in ARDS resulting from COVID-19 compared to other causes of ARDS, such as bacterial sepsis is unclear. Moreover, the beneficial effects of dexamethasone therapy during severe COVID-19 remain speculative, but understanding the mechanistic effects could improve evidence-based therapeutic interventions. To interrogate these relationships, we developed an scRNAseq atlas that is freely accessible (biernaskielab.ca/COVID_neutrophil). We discovered that compared to bacterial ARDS, COVID-19 was associated with distinct neutrophil polarization characterized by either interferon (IFN) or prostaglandin (PG) active states. Neutrophils from bacterial ARDS had higher expression of antibacterial molecules such as PLAC8 and CD83. Dexamethasone therapy in COVID patients rapidly altered the IFNactive state, downregulated interferon responsive genes, and activated IL1R2+ve neutrophils. Dexamethasone also induced the emergence of immature neutrophils expressing immunosuppressive molecules ARG1 and ANXA1, which were not present in healthy controls. Moreover, dexamethasone remodeled global cellular interactions by changing neutrophils from information receivers into information providers. Importantly, male patients had higher proportions of IFNactive neutrophils and a greater degree of steroid-induced immature neutrophil expansion. Indeed, the highest proportion of IFNactive neutrophils was associated with mortality. These results define neutrophil states unique to COVID-19 when contextualized to other life-threatening infections, thereby enhancing the relevance of our findings at the bedside. Furthermore, the molecular benefits of dexamethasone therapy are also defined. The identified molecular pathways can now be targeted to develop improved therapeutics.
HostingRepositoryPRIDE
AnnounceDate2021-10-05
AnnouncementXMLSubmission_2021-10-05_06:16:38.612.xml
DigitalObjectIdentifier
ReviewLevelPeer-reviewed dataset
DatasetOriginOriginal dataset
RepositorySupportUnsupported dataset by repository
PrimarySubmitterLuiz Gustavo de Almeida
SpeciesList scientific name: Homo sapiens (Human); NCBI TaxID: 9606;
ModificationListacetylated residue; monohydroxylated residue; iodoacetamide derivatized residue; deamidated residue
InstrumentOrbitrap Fusion Lumos
Dataset History
RevisionDatetimeStatusChangeLog Entry
02021-09-09 13:49:49ID requested
12021-10-05 06:16:38announced
Publication List
Dataset with its publication pending
Keyword List
submitter keyword: Human, serum, COVID-19, bacterial ARDS, neutrophil, LC-MSMS, Orbitrap, Maxquant
Contact List
Jeff Biernaskie
contact affiliationDepartment of Comparative Biology and Experimental Medicine, Faculty of Veterinary Medicine, University of Calgary; Hotchkiss Brain Institute, University of Calgary; Alberta Children’s Hospital Research Institute, University of Calgary
contact emailjabierna@ucalgary.ca
lab head
Luiz Gustavo de Almeida
contact affiliationUniversity of Calgary
contact emailluizgustavo.biotec@hotmail.com
dataset submitter
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Dataset FTP location
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