Early stimulated immune responses predict clinical disease severity in hospitalized COVID-19 patients
Background The immune pathogenesis underlying the diverse clinical course of COVID-19 is poorly understood. Currently, there is an unmet need in daily clinical practice for early biomarkers and improved risk stratification tools to help identify and monitor COVID-19 patients at risk of severe diseas...
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| Published in: | Communications medicine Vol. 2; no. 1; p. 114 |
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| Main Authors: | , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
London
Nature Publishing Group UK
12.09.2022
Springer Nature B.V Nature Portfolio |
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| ISSN: | 2730-664X, 2730-664X |
| Online Access: | Get full text |
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| Abstract | Background
The immune pathogenesis underlying the diverse clinical course of COVID-19 is poorly understood. Currently, there is an unmet need in daily clinical practice for early biomarkers and improved risk stratification tools to help identify and monitor COVID-19 patients at risk of severe disease.
Methods
We performed longitudinal assessment of stimulated immune responses in 30 patients hospitalized with COVID-19. We used the TruCulture whole-blood ligand-stimulation assay applying standardized stimuli to activate distinct immune pathways, allowing quantification of cytokine responses. We further characterized immune cell subsets by flow cytometry and used this deep immunophenotyping data to map the course of clinical disease within and between patients.
Results
Here we demonstrate impairments in innate immune response pathways at time of COVID-19 hospitalization that are associated with the development of severe disease. We show that these impairments are transient in those discharged from hospital, as illustrated by functional and cellular immune reconstitution. Specifically, we identify lower levels of LPS-stimulated IL-1β, and R848-stimulated IL-12 and IL-17A, at hospital admission to be significantly associated with increasing COVID-19 disease severity during hospitalization. Furthermore, we propose a stimulated immune response signature for predicting risk of developing severe or critical COVID-19 disease at time of hospitalization, to validate in larger cohorts.
Conclusions
We identify early impairments in innate immune responses that are associated with subsequent COVID-19 disease severity. Our findings provide basis for early identification of patients at risk of severe disease which may have significant implications for the early management of patients hospitalized with COVID-19.
Plain language summary
The manifestation of COVID-19 varies from asymptomatic to severe pneumonia requiring ventilator support or multi-organ failure. It is still poorly understood how the immune response to SARS-CoV-2 affects the development of severe disease. There is also a lack of clinical tools to identify patients early with high risk of poor outcome. Here, we looked for potential markers of disease severity in hospitalized COVID-19 patients using method to measure individual immune reactions. We found associations between impaired immune response pathways at time of hospitalization and development of severe and critical COVID-19 disease, and we identified a number of immune markers that could be used to predict poor outcome. Our findings could help identify at-risk patients upon hospitalization, enabling closer monitoring and earlier interventions.
Svanberg et al. longitudinally assess the immune response in patients with COVID-19. The authors report specific immune parameters associated with the development of severe disease. |
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| AbstractList | BackgroundThe immune pathogenesis underlying the diverse clinical course of COVID-19 is poorly understood. Currently, there is an unmet need in daily clinical practice for early biomarkers and improved risk stratification tools to help identify and monitor COVID-19 patients at risk of severe disease.MethodsWe performed longitudinal assessment of stimulated immune responses in 30 patients hospitalized with COVID-19. We used the TruCulture whole-blood ligand-stimulation assay applying standardized stimuli to activate distinct immune pathways, allowing quantification of cytokine responses. We further characterized immune cell subsets by flow cytometry and used this deep immunophenotyping data to map the course of clinical disease within and between patients.ResultsHere we demonstrate impairments in innate immune response pathways at time of COVID-19 hospitalization that are associated with the development of severe disease. We show that these impairments are transient in those discharged from hospital, as illustrated by functional and cellular immune reconstitution. Specifically, we identify lower levels of LPS-stimulated IL-1β, and R848-stimulated IL-12 and IL-17A, at hospital admission to be significantly associated with increasing COVID-19 disease severity during hospitalization. Furthermore, we propose a stimulated immune response signature for predicting risk of developing severe or critical COVID-19 disease at time of hospitalization, to validate in larger cohorts.ConclusionsWe identify early impairments in innate immune responses that are associated with subsequent COVID-19 disease severity. Our findings provide basis for early identification of patients at risk of severe disease which may have significant implications for the early management of patients hospitalized with COVID-19.Plain language summaryThe manifestation of COVID-19 varies from asymptomatic to severe pneumonia requiring ventilator support or multi-organ failure. It is still poorly understood how the immune response to SARS-CoV-2 affects the development of severe disease. There is also a lack of clinical tools to identify patients early with high risk of poor outcome. Here, we looked for potential markers of disease severity in hospitalized COVID-19 patients using method to measure individual immune reactions. We found associations between impaired immune response pathways at time of hospitalization and development of severe and critical COVID-19 disease, and we identified a number of immune markers that could be used to predict poor outcome. Our findings could help identify at-risk patients upon hospitalization, enabling closer monitoring and earlier interventions. The immune pathogenesis underlying the diverse clinical course of COVID-19 is poorly understood. Currently, there is an unmet need in daily clinical practice for early biomarkers and improved risk stratification tools to help identify and monitor COVID-19 patients at risk of severe disease.BackgroundThe immune pathogenesis underlying the diverse clinical course of COVID-19 is poorly understood. Currently, there is an unmet need in daily clinical practice for early biomarkers and improved risk stratification tools to help identify and monitor COVID-19 patients at risk of severe disease.We performed longitudinal assessment of stimulated immune responses in 30 patients hospitalized with COVID-19. We used the TruCulture whole-blood ligand-stimulation assay applying standardized stimuli to activate distinct immune pathways, allowing quantification of cytokine responses. We further characterized immune cell subsets by flow cytometry and used this deep immunophenotyping data to map the course of clinical disease within and between patients.MethodsWe performed longitudinal assessment of stimulated immune responses in 30 patients hospitalized with COVID-19. We used the TruCulture whole-blood ligand-stimulation assay applying standardized stimuli to activate distinct immune pathways, allowing quantification of cytokine responses. We further characterized immune cell subsets by flow cytometry and used this deep immunophenotyping data to map the course of clinical disease within and between patients.Here we demonstrate impairments in innate immune response pathways at time of COVID-19 hospitalization that are associated with the development of severe disease. We show that these impairments are transient in those discharged from hospital, as illustrated by functional and cellular immune reconstitution. Specifically, we identify lower levels of LPS-stimulated IL-1β, and R848-stimulated IL-12 and IL-17A, at hospital admission to be significantly associated with increasing COVID-19 disease severity during hospitalization. Furthermore, we propose a stimulated immune response signature for predicting risk of developing severe or critical COVID-19 disease at time of hospitalization, to validate in larger cohorts.ResultsHere we demonstrate impairments in innate immune response pathways at time of COVID-19 hospitalization that are associated with the development of severe disease. We show that these impairments are transient in those discharged from hospital, as illustrated by functional and cellular immune reconstitution. Specifically, we identify lower levels of LPS-stimulated IL-1β, and R848-stimulated IL-12 and IL-17A, at hospital admission to be significantly associated with increasing COVID-19 disease severity during hospitalization. Furthermore, we propose a stimulated immune response signature for predicting risk of developing severe or critical COVID-19 disease at time of hospitalization, to validate in larger cohorts.We identify early impairments in innate immune responses that are associated with subsequent COVID-19 disease severity. Our findings provide basis for early identification of patients at risk of severe disease which may have significant implications for the early management of patients hospitalized with COVID-19.ConclusionsWe identify early impairments in innate immune responses that are associated with subsequent COVID-19 disease severity. Our findings provide basis for early identification of patients at risk of severe disease which may have significant implications for the early management of patients hospitalized with COVID-19. Background The immune pathogenesis underlying the diverse clinical course of COVID-19 is poorly understood. Currently, there is an unmet need in daily clinical practice for early biomarkers and improved risk stratification tools to help identify and monitor COVID-19 patients at risk of severe disease. Methods We performed longitudinal assessment of stimulated immune responses in 30 patients hospitalized with COVID-19. We used the TruCulture whole-blood ligand-stimulation assay applying standardized stimuli to activate distinct immune pathways, allowing quantification of cytokine responses. We further characterized immune cell subsets by flow cytometry and used this deep immunophenotyping data to map the course of clinical disease within and between patients. Results Here we demonstrate impairments in innate immune response pathways at time of COVID-19 hospitalization that are associated with the development of severe disease. We show that these impairments are transient in those discharged from hospital, as illustrated by functional and cellular immune reconstitution. Specifically, we identify lower levels of LPS-stimulated IL-1β, and R848-stimulated IL-12 and IL-17A, at hospital admission to be significantly associated with increasing COVID-19 disease severity during hospitalization. Furthermore, we propose a stimulated immune response signature for predicting risk of developing severe or critical COVID-19 disease at time of hospitalization, to validate in larger cohorts. Conclusions We identify early impairments in innate immune responses that are associated with subsequent COVID-19 disease severity. Our findings provide basis for early identification of patients at risk of severe disease which may have significant implications for the early management of patients hospitalized with COVID-19. Plain language summary The manifestation of COVID-19 varies from asymptomatic to severe pneumonia requiring ventilator support or multi-organ failure. It is still poorly understood how the immune response to SARS-CoV-2 affects the development of severe disease. There is also a lack of clinical tools to identify patients early with high risk of poor outcome. Here, we looked for potential markers of disease severity in hospitalized COVID-19 patients using method to measure individual immune reactions. We found associations between impaired immune response pathways at time of hospitalization and development of severe and critical COVID-19 disease, and we identified a number of immune markers that could be used to predict poor outcome. Our findings could help identify at-risk patients upon hospitalization, enabling closer monitoring and earlier interventions. Svanberg et al. longitudinally assess the immune response in patients with COVID-19. The authors report specific immune parameters associated with the development of severe disease. The manifestation of COVID-19 varies from asymptomatic to severe pneumonia requiring ventilator support or multi-organ failure. It is still poorly understood how the immune response to SARS-CoV-2 affects the development of severe disease. There is also a lack of clinical tools to identify patients early with high risk of poor outcome. Here, we looked for potential markers of disease severity in hospitalized COVID-19 patients using method to measure individual immune reactions. We found associations between impaired immune response pathways at time of hospitalization and development of severe and critical COVID-19 disease, and we identified a number of immune markers that could be used to predict poor outcome. Our findings could help identify at-risk patients upon hospitalization, enabling closer monitoring and earlier interventions. Svanberg et al. longitudinally assess the immune response in patients with COVID-19. The authors report specific immune parameters associated with the development of severe disease. BACKGROUNDThe immune pathogenesis underlying the diverse clinical course of COVID-19 is poorly understood. Currently, there is an unmet need in daily clinical practice for early biomarkers and improved risk stratification tools to help identify and monitor COVID-19 patients at risk of severe disease.METHODSWe performed longitudinal assessment of stimulated immune responses in 30 patients hospitalized with COVID-19. We used the TruCulture whole-blood ligand-stimulation assay applying standardized stimuli to activate distinct immune pathways, allowing quantification of cytokine responses. We further characterized immune cell subsets by flow cytometry and used this deep immunophenotyping data to map the course of clinical disease within and between patients.RESULTSHere we demonstrate impairments in innate immune response pathways at time of COVID-19 hospitalization that are associated with the development of severe disease. We show that these impairments are transient in those discharged from hospital, as illustrated by functional and cellular immune reconstitution. Specifically, we identify lower levels of LPS-stimulated IL-1β, and R848-stimulated IL-12 and IL-17A, at hospital admission to be significantly associated with increasing COVID-19 disease severity during hospitalization. Furthermore, we propose a stimulated immune response signature for predicting risk of developing severe or critical COVID-19 disease at time of hospitalization, to validate in larger cohorts.CONCLUSIONSWe identify early impairments in innate immune responses that are associated with subsequent COVID-19 disease severity. Our findings provide basis for early identification of patients at risk of severe disease which may have significant implications for the early management of patients hospitalized with COVID-19. Svanberg et al. longitudinally assess the immune response in patients with COVID-19. The authors report specific immune parameters associated with the development of severe disease. The immune pathogenesis underlying the diverse clinical course of COVID-19 is poorly understood. Currently, there is an unmet need in daily clinical practice for early biomarkers and improved risk stratification tools to help identify and monitor COVID-19 patients at risk of severe disease. We performed longitudinal assessment of stimulated immune responses in 30 patients hospitalized with COVID-19. We used the TruCulture whole-blood ligand-stimulation assay applying standardized stimuli to activate distinct immune pathways, allowing quantification of cytokine responses. We further characterized immune cell subsets by flow cytometry and used this deep immunophenotyping data to map the course of clinical disease within and between patients. Here we demonstrate impairments in innate immune response pathways at time of COVID-19 hospitalization that are associated with the development of severe disease. We show that these impairments are transient in those discharged from hospital, as illustrated by functional and cellular immune reconstitution. Specifically, we identify lower levels of LPS-stimulated IL-1β, and R848-stimulated IL-12 and IL-17A, at hospital admission to be significantly associated with increasing COVID-19 disease severity during hospitalization. Furthermore, we propose a stimulated immune response signature for predicting risk of developing severe or critical COVID-19 disease at time of hospitalization, to validate in larger cohorts. We identify early impairments in innate immune responses that are associated with subsequent COVID-19 disease severity. Our findings provide basis for early identification of patients at risk of severe disease which may have significant implications for the early management of patients hospitalized with COVID-19. |
| ArticleNumber | 114 |
| Author | Gjærde, Lars Klingen MacPherson, Cameron Lindegaard, Birgitte Zucco, Adrian Brooks, Patrick Terrence Nielsen, Susanne Dam Agius, Rudi Ostrowski, Sisse Rye Hald, Annemette Harboe, Zitta Barrella Podlekareva, Daria Bay, Jakob Thaning Gang, Anne Ortved da Cunha-Bang, Caspar Lundgren, Jens Lebech, Anne-Mette Hersby, Ditte Stampe Brieghel, Christian Marquart, Hanne Svanberg, Rebecka Sejdic, Adin Helleberg, Marie Andersen, Michael Asger Møller, Maria Elizabeth Engel Niemann, Carsten Utoft Faitova, Tereza |
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Department of Hematology, Copenhagen University Hospital, Rigshospitalet – sequence: 7 givenname: Caspar surname: da Cunha-Bang fullname: da Cunha-Bang, Caspar organization: Department of Hematology, Copenhagen University Hospital, Rigshospitalet – sequence: 8 givenname: Lars Klingen orcidid: 0000-0002-5496-9955 surname: Gjærde fullname: Gjærde, Lars Klingen organization: Department of Hematology, Copenhagen University Hospital, Rigshospitalet – sequence: 9 givenname: Maria Elizabeth Engel surname: Møller fullname: Møller, Maria Elizabeth Engel organization: Department of Clinical Immunology, Copenhagen University Hospital, Rigshospitalet – sequence: 10 givenname: Patrick Terrence surname: Brooks fullname: Brooks, Patrick Terrence organization: Department of Clinical Immunology, Copenhagen University Hospital, Rigshospitalet – sequence: 11 givenname: Birgitte surname: Lindegaard fullname: Lindegaard, Birgitte organization: Department of Pulmonary and Infectious Diseases, Copenhagen 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0000-0001-6906-8159 surname: Hald fullname: Hald, Annemette organization: Department of Infectious Diseases, Copenhagen University Hospital, Rigshospitalet – sequence: 20 givenname: Jakob Thaning surname: Bay fullname: Bay, Jakob Thaning organization: Department of Clinical Immunology, Copenhagen University Hospital, Rigshospitalet – sequence: 21 givenname: Hanne orcidid: 0000-0001-9740-6522 surname: Marquart fullname: Marquart, Hanne organization: Department of Clinical Immunology, Copenhagen University Hospital, Rigshospitalet – sequence: 22 givenname: Jens orcidid: 0000-0001-8901-7850 surname: Lundgren fullname: Lundgren, Jens organization: PERSIMUNE Center of Excellence, Copenhagen University Hospital, Rigshospitalet, Department of Clinical Medicine, University of Copenhagen, Department of Infectious Diseases, Copenhagen University Hospital, Rigshospitalet – sequence: 23 givenname: Anne-Mette surname: Lebech fullname: Lebech, Anne-Mette organization: Department of Clinical Medicine, University of Copenhagen, Department of Infectious Diseases, Copenhagen University Hospital, Rigshospitalet – sequence: 24 givenname: Marie surname: Helleberg fullname: Helleberg, Marie organization: PERSIMUNE Center of Excellence, Copenhagen University Hospital, Rigshospitalet, Department of Infectious Diseases, Copenhagen University Hospital, Rigshospitalet – sequence: 25 givenname: Carsten Utoft orcidid: 0000-0001-9880-5242 surname: Niemann fullname: Niemann, Carsten Utoft organization: Department of Hematology, Copenhagen University Hospital, Rigshospitalet, Department of Clinical Medicine, University of Copenhagen – sequence: 26 givenname: Sisse Rye orcidid: 0000-0001-5288-3851 surname: Ostrowski fullname: Ostrowski, Sisse Rye email: sisse.rye.ostrowski@regionh.dk organization: Department of Clinical Immunology, Copenhagen University Hospital, Rigshospitalet, Department of Clinical Medicine, University of Copenhagen |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/36101705$$D View this record in MEDLINE/PubMed |
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| Keywords | Innate immunity Viral infection |
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| Snippet | Background
The immune pathogenesis underlying the diverse clinical course of COVID-19 is poorly understood. Currently, there is an unmet need in daily clinical... The immune pathogenesis underlying the diverse clinical course of COVID-19 is poorly understood. Currently, there is an unmet need in daily clinical practice... BackgroundThe immune pathogenesis underlying the diverse clinical course of COVID-19 is poorly understood. Currently, there is an unmet need in daily clinical... BACKGROUNDThe immune pathogenesis underlying the diverse clinical course of COVID-19 is poorly understood. Currently, there is an unmet need in daily clinical... The manifestation of COVID-19 varies from asymptomatic to severe pneumonia requiring ventilator support or multi-organ failure. It is still poorly understood... Svanberg et al. longitudinally assess the immune response in patients with COVID-19. The authors report specific immune parameters associated with the... |
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| SubjectTerms | 13/31 631/250/255/2514 631/250/262 96/21 Biomarkers Coronaviruses COVID-19 Cytokines Flow cytometry Hospitalization Immune response Infections Intensive care Medicine Medicine & Public Health Pandemics Patients Severe acute respiratory syndrome coronavirus 2 T cell receptors Tumor necrosis factor-TNF Ventilators |
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| Title | Early stimulated immune responses predict clinical disease severity in hospitalized COVID-19 patients |
| URI | https://link.springer.com/article/10.1038/s43856-022-00178-5 https://www.ncbi.nlm.nih.gov/pubmed/36101705 https://www.proquest.com/docview/2771831643 https://www.proquest.com/docview/2714391949 https://www.proquest.com/docview/2738192080 https://pubmed.ncbi.nlm.nih.gov/PMC9466310 https://doaj.org/article/bd613745fba3483e88dcd4c9630cbdab |
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