An immune-based biomarker signature is associated with mortality in COVID-19 patients
Immune and inflammatory responses to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) contribute to disease severity of coronavirus disease 2019 (COVID-19). However, the utility of specific immune-based biomarkers to predict clinical outcome remains elusive. Here, we analyzed levels of 6...
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| Veröffentlicht in: | JCI insight Jg. 6; H. 1 |
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| Format: | Journal Article |
| Sprache: | Englisch |
| Veröffentlicht: |
United States
American Society for Clinical Investigation
11.01.2021
American Society for Clinical investigation |
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| ISSN: | 2379-3708, 2379-3708 |
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| Abstract | Immune and inflammatory responses to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) contribute to disease severity of coronavirus disease 2019 (COVID-19). However, the utility of specific immune-based biomarkers to predict clinical outcome remains elusive. Here, we analyzed levels of 66 soluble biomarkers in 175 Italian patients with COVID-19 ranging from mild/moderate to critical severity and assessed type I IFN-, type II IFN-, and NF-κB-dependent whole-blood transcriptional signatures. A broad inflammatory signature was observed, implicating activation of various immune and nonhematopoietic cell subsets. Discordance between IFN-α2a protein and IFNA2 transcript levels in blood suggests that type I IFNs during COVID-19 may be primarily produced by tissue-resident cells. Multivariable analysis of patients' first samples revealed 12 biomarkers (CCL2, IL-15, soluble ST2 [sST2], NGAL, sTNFRSF1A, ferritin, IL-6, S100A9, MMP-9, IL-2, sVEGFR1, IL-10) that when increased were independently associated with mortality. Multivariate analyses of longitudinal biomarker trajectories identified 8 of the aforementioned biomarkers (IL-15, IL-2, NGAL, CCL2, MMP-9, sTNFRSF1A, sST2, IL-10) and 2 additional biomarkers (lactoferrin, CXCL9) that were substantially associated with mortality when increased, while IL-1α was associated with mortality when decreased. Among these, sST2, sTNFRSF1A, IL-10, and IL-15 were consistently higher throughout the hospitalization in patients who died versus those who recovered, suggesting that these biomarkers may provide an early warning of eventual disease outcome. |
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| AbstractList | Immune and inflammatory responses to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) contribute to disease severity of coronavirus disease 2019 (COVID-19). However, the utility of specific immune-based biomarkers to predict clinical outcome remains elusive. Here, we analyzed levels of 66 soluble biomarkers in 175 Italian patients with COVID-19 ranging from mild/moderate to critical severity and assessed type I IFN-, type II IFN-, and NF-κB-dependent whole-blood transcriptional signatures. A broad inflammatory signature was observed, implicating activation of various immune and nonhematopoietic cell subsets. Discordance between IFN-α2a protein and IFNA2 transcript levels in blood suggests that type I IFNs during COVID-19 may be primarily produced by tissue-resident cells. Multivariable analysis of patients' first samples revealed 12 biomarkers (CCL2, IL-15, soluble ST2 [sST2], NGAL, sTNFRSF1A, ferritin, IL-6, S100A9, MMP-9, IL-2, sVEGFR1, IL-10) that when increased were independently associated with mortality. Multivariate analyses of longitudinal biomarker trajectories identified 8 of the aforementioned biomarkers (IL-15, IL-2, NGAL, CCL2, MMP-9, sTNFRSF1A, sST2, IL-10) and 2 additional biomarkers (lactoferrin, CXCL9) that were substantially associated with mortality when increased, while IL-1α was associated with mortality when decreased. Among these, sST2, sTNFRSF1A, IL-10, and IL-15 were consistently higher throughout the hospitalization in patients who died versus those who recovered, suggesting that these biomarkers may provide an early warning of eventual disease outcome. Immune and inflammatory responses to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) contribute to disease severity of coronavirus disease 2019 (COVID-19). However, the utility of specific immune-based biomarkers to predict clinical outcome remains elusive. Here, we analyzed levels of 66 soluble biomarkers in 175 Italian patients with COVID-19 ranging from mild/moderate to critical severity and assessed type I IFN-, type II IFN-, and NF-κB-dependent whole-blood transcriptional signatures. A broad inflammatory signature was observed, implicating activation of various immune and nonhematopoietic cell subsets. Discordance between IFN-α2a protein and IFNA2 transcript levels in blood suggests that type I IFNs during COVID-19 may be primarily produced by tissue-resident cells. Multivariable analysis of patients' first samples revealed 12 biomarkers (CCL2, IL-15, soluble ST2 [sST2], NGAL, sTNFRSF1A, ferritin, IL-6, S100A9, MMP-9, IL-2, sVEGFR1, IL-10) that when increased were independently associated with mortality. Multivariate analyses of longitudinal biomarker trajectories identified 8 of the aforementioned biomarkers (IL-15, IL-2, NGAL, CCL2, MMP-9, sTNFRSF1A, sST2, IL-10) and 2 additional biomarkers (lactoferrin, CXCL9) that were substantially associated with mortality when increased, while IL-1α was associated with mortality when decreased. Among these, sST2, sTNFRSF1A, IL-10, and IL-15 were consistently higher throughout the hospitalization in patients who died versus those who recovered, suggesting that these biomarkers may provide an early warning of eventual disease outcome.Immune and inflammatory responses to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) contribute to disease severity of coronavirus disease 2019 (COVID-19). However, the utility of specific immune-based biomarkers to predict clinical outcome remains elusive. Here, we analyzed levels of 66 soluble biomarkers in 175 Italian patients with COVID-19 ranging from mild/moderate to critical severity and assessed type I IFN-, type II IFN-, and NF-κB-dependent whole-blood transcriptional signatures. A broad inflammatory signature was observed, implicating activation of various immune and nonhematopoietic cell subsets. Discordance between IFN-α2a protein and IFNA2 transcript levels in blood suggests that type I IFNs during COVID-19 may be primarily produced by tissue-resident cells. Multivariable analysis of patients' first samples revealed 12 biomarkers (CCL2, IL-15, soluble ST2 [sST2], NGAL, sTNFRSF1A, ferritin, IL-6, S100A9, MMP-9, IL-2, sVEGFR1, IL-10) that when increased were independently associated with mortality. Multivariate analyses of longitudinal biomarker trajectories identified 8 of the aforementioned biomarkers (IL-15, IL-2, NGAL, CCL2, MMP-9, sTNFRSF1A, sST2, IL-10) and 2 additional biomarkers (lactoferrin, CXCL9) that were substantially associated with mortality when increased, while IL-1α was associated with mortality when decreased. Among these, sST2, sTNFRSF1A, IL-10, and IL-15 were consistently higher throughout the hospitalization in patients who died versus those who recovered, suggesting that these biomarkers may provide an early warning of eventual disease outcome. |
| Author | Bonfanti, Paolo Burbelo, Peter D. Brugnoni, Duilio Delmonte, Ottavia M. Castagnoli, Riccardo Kahle, Dana E. Su, Helen C. Rastegar, Andre T. Alehashemi, Sara Desai, Jigar V. Sottini, Alessandra Oikonomou, Vasileios Shakoory, Bita Imberti, Luisa Cohen, Jeffrey I. Fintzi, Jonathan Stack, Michael Bettini, Laura Rachele Quiros-Roldan, Eugenia Lionakis, Michail S. Gliniewicz, Emily F. Gallin, John I. Fink, Danielle L. Montagna, Daniela Biondi, Andrea Notarangelo, Luigi D. Kuhns, Douglas B. Dobbs, Kerry Ricotta, Emily E. Shaw, Elana Tsang, John S. Rossi, Camillo D’Angio’, Mariella Myint-Hpu, Katherine Goldbach-Mansky, Raphaela Zarember, Kol A. de Jesus, Adriana A. Almeida Castelli, Francesco Canna, Scott W. Chertow, Daniel W. Levinson, Susan L. Licari, Amelia Calvo, Katherine R. DiNubile, Mark J. Abers, Michael S. Marseglia, Gian Luigi |
| AuthorAffiliation | 10 Department of Infectious Diseases, San Gerardo Hospital, University of Milano-Bicocca, Monza, Italy 14 BioAegis Therapeutics, Inc, North Brunswick, New Jersey, USA 21 The NIAID COVID-19 Consortium is detailed in Supplemental Acknowledgments 17 Laboratory of Infectious Diseases, NIAID, NIH, Bethesda, Maryland, USA 1 Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, Maryland, USA 11 Department of Pediatrics and 7 Direzione Sanitaria, ASST Spedali Civili di Brescia, Italy 18 Hematology Section, Department of Laboratory Medicine, NIH Clinical Center, NIH, Bethesda, Maryland, USA 5 CREA Laboratory, Diagnostic Department, ASST Spedali Civili di Brescia, Brescia, Italy 12 Laboratory of Immunology and Transplantation, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy 4 Children’s Hospital of Pittsburgh, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA 20 Center for |
| AuthorAffiliation_xml | – name: 4 Children’s Hospital of Pittsburgh, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA – name: 11 Department of Pediatrics and – name: 10 Department of Infectious Diseases, San Gerardo Hospital, University of Milano-Bicocca, Monza, Italy – name: 16 National Institute of Dental and Craniofacial Research, NIH, Bethesda, Maryland, USA – name: 19 Laboratory of Immune System Biology and Clinical Genomics Program, NIAID, NIH, Bethesda, Maryland, USA – name: 14 BioAegis Therapeutics, Inc, North Brunswick, New Jersey, USA – name: 5 CREA Laboratory, Diagnostic Department, ASST Spedali Civili di Brescia, Brescia, Italy – name: 21 The NIAID COVID-19 Consortium is detailed in Supplemental Acknowledgments – name: 7 Direzione Sanitaria, ASST Spedali Civili di Brescia, Italy – name: 6 Department of Infectious and Tropical Diseases, University of Brescia and ASST Spedali Civili di Brescia, Brescia, Italy – name: 9 Pediatric Department and Centro Tettamanti-European Reference Network on Paediatric Cancer, European Reference Network on Haematological Diseases, and European Reference Network on Hereditary Metabolic Disorders-University of Milano-Bicocca-Fondazione MBBM, Monza, Italy – name: 13 Department of Clinical, Surgical, Diagnostic and Pediatric Sciences, University of Pavia, Pavia, Italy – name: 17 Laboratory of Infectious Diseases, NIAID, NIH, Bethesda, Maryland, USA – name: 1 Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, Maryland, USA – name: 12 Laboratory of Immunology and Transplantation, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy – name: 15 Critical Care Medicine Department, NIH Clinical Center, NIH, Bethesda, Maryland, USA – name: 20 Center for Human Immunology, Autoimmunity, and Inflammation, NIAID, NIH, Bethesda, Maryland, USA – name: 3 Neutrophil Monitoring Laboratory, Leidos Biomedical Research, Inc, Frederick National Laboratory for Cancer Research, Frederick, Maryland, USA – name: 18 Hematology Section, Department of Laboratory Medicine, NIH Clinical Center, NIH, Bethesda, Maryland, USA – name: 2 Biostatistics Research Branch, NIAID, NIH, Bethesda, Maryland, USA – name: 8 Laboratorio Analisi Chimico-Cliniche, ASST Spedali Civili, Brescia, Italy |
| Author_xml | – sequence: 1 givenname: Michael S. orcidid: 0000-0003-2234-2813 surname: Abers fullname: Abers, Michael S. – sequence: 2 givenname: Ottavia M. orcidid: 0000-0002-4772-0799 surname: Delmonte fullname: Delmonte, Ottavia M. – sequence: 3 givenname: Emily E. orcidid: 0000-0001-9928-8275 surname: Ricotta fullname: Ricotta, Emily E. – sequence: 4 givenname: Jonathan surname: Fintzi fullname: Fintzi, Jonathan – sequence: 5 givenname: Danielle L. surname: Fink fullname: Fink, Danielle L. – sequence: 6 givenname: Adriana A. Almeida surname: de Jesus fullname: de Jesus, Adriana A. Almeida – sequence: 7 givenname: Kol A. orcidid: 0000-0002-9624-7096 surname: Zarember fullname: Zarember, Kol A. – sequence: 8 givenname: Sara orcidid: 0000-0002-6531-6108 surname: Alehashemi fullname: Alehashemi, Sara – sequence: 9 givenname: Vasileios orcidid: 0000-0002-7553-0159 surname: Oikonomou fullname: Oikonomou, Vasileios – sequence: 10 givenname: Jigar V. orcidid: 0000-0002-8823-0796 surname: Desai fullname: Desai, Jigar V. – sequence: 11 givenname: Scott W. orcidid: 0000-0003-3837-5337 surname: Canna fullname: Canna, Scott W. – sequence: 12 givenname: Bita orcidid: 0000-0003-4615-370X surname: Shakoory fullname: Shakoory, Bita – sequence: 13 givenname: Kerry orcidid: 0000-0002-3432-3137 surname: Dobbs fullname: Dobbs, Kerry – sequence: 14 givenname: Luisa surname: Imberti fullname: Imberti, Luisa – sequence: 15 givenname: Alessandra surname: Sottini fullname: Sottini, Alessandra – sequence: 16 givenname: Eugenia surname: Quiros-Roldan fullname: Quiros-Roldan, Eugenia – sequence: 17 givenname: Francesco surname: Castelli fullname: Castelli, Francesco – sequence: 18 givenname: Camillo orcidid: 0000-0001-9271-813X surname: Rossi fullname: Rossi, Camillo – sequence: 19 givenname: Duilio orcidid: 0000-0001-9420-9961 surname: Brugnoni fullname: Brugnoni, Duilio – sequence: 20 givenname: Andrea surname: Biondi fullname: Biondi, Andrea – sequence: 21 givenname: Laura Rachele surname: Bettini fullname: Bettini, Laura Rachele – sequence: 22 givenname: Mariella surname: D’Angio’ fullname: D’Angio’, Mariella – sequence: 23 givenname: Paolo orcidid: 0000-0001-7289-8823 surname: Bonfanti fullname: Bonfanti, Paolo – sequence: 24 givenname: Riccardo orcidid: 0000-0003-0029-9383 surname: Castagnoli fullname: Castagnoli, Riccardo – sequence: 25 givenname: Daniela surname: Montagna fullname: Montagna, Daniela – sequence: 26 givenname: Amelia orcidid: 0000-0002-1773-6482 surname: Licari fullname: Licari, Amelia – sequence: 27 givenname: Gian Luigi orcidid: 0000-0003-0029-9383 surname: Marseglia fullname: Marseglia, Gian Luigi – sequence: 28 givenname: Emily F. surname: Gliniewicz fullname: Gliniewicz, Emily F. – sequence: 29 givenname: Elana surname: Shaw fullname: Shaw, Elana – sequence: 30 givenname: Dana E. surname: Kahle fullname: Kahle, Dana E. – sequence: 31 givenname: Andre T. orcidid: 0000-0003-4724-9041 surname: Rastegar fullname: Rastegar, Andre T. – sequence: 32 givenname: Michael surname: Stack fullname: Stack, Michael – sequence: 33 givenname: Katherine surname: Myint-Hpu fullname: Myint-Hpu, Katherine – sequence: 34 givenname: Susan L. orcidid: 0000-0001-7902-1274 surname: Levinson fullname: Levinson, Susan L. – sequence: 35 givenname: Mark J. surname: DiNubile fullname: DiNubile, Mark J. – sequence: 36 givenname: Daniel W. orcidid: 0000-0002-1675-1728 surname: Chertow fullname: Chertow, Daniel W. – sequence: 37 givenname: Peter D. surname: Burbelo fullname: Burbelo, Peter D. – sequence: 38 givenname: Jeffrey I. surname: Cohen fullname: Cohen, Jeffrey I. – sequence: 39 givenname: Katherine R. orcidid: 0000-0002-0771-4191 surname: Calvo fullname: Calvo, Katherine R. – sequence: 40 givenname: John S. orcidid: 0000-0003-3186-3047 surname: Tsang fullname: Tsang, John S. – sequence: 41 givenname: Helen C. orcidid: 0000-0002-5582-9110 surname: Su fullname: Su, Helen C. – sequence: 42 givenname: John I. surname: Gallin fullname: Gallin, John I. – sequence: 43 givenname: Douglas B. orcidid: 0000-0002-9971-0760 surname: Kuhns fullname: Kuhns, Douglas B. – sequence: 44 givenname: Raphaela surname: Goldbach-Mansky fullname: Goldbach-Mansky, Raphaela – sequence: 45 givenname: Michail S. surname: Lionakis fullname: Lionakis, Michail S. – sequence: 46 givenname: Luigi D. surname: Notarangelo fullname: Notarangelo, Luigi D. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33232303$$D View this record in MEDLINE/PubMed |
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| Title | An immune-based biomarker signature is associated with mortality in COVID-19 patients |
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