Pro- and Anti-Inflammatory Responses in Severe COVID-19-Induced Acute Respiratory Distress Syndrome—An Observational Pilot Study
The severity of Coronavirus Disease 2019 (COVID-19) is largely determined by the immune response. First studies indicate altered lymphocyte counts and function. However, interactions of pro- and anti-inflammatory mechanisms remain elusive. In the current study we characterized the immune responses i...
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| Vydáno v: | Frontiers in immunology Ročník 11; s. 581338 |
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Frontiers Media S.A
06.10.2020
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| ISSN: | 1664-3224, 1664-3224 |
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| Abstract | The severity of Coronavirus Disease 2019 (COVID-19) is largely determined by the immune response. First studies indicate altered lymphocyte counts and function. However, interactions of pro- and anti-inflammatory mechanisms remain elusive. In the current study we characterized the immune responses in patients suffering from severe COVID-19-induced acute respiratory distress syndrome (ARDS).
This was a single-center retrospective study in patients admitted to the intensive care unit (ICU) with confirmed COVID-19 between March 14
and May 28
2020 (n = 39). Longitudinal data were collected within routine clinical care, including flow-cytometry of lymphocyte subsets, cytokine analysis and growth differentiation factor 15 (GDF-15). Antibody responses against the receptor binding domain (RBD) of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Spike protein were analyzed.
All patients suffered from severe ARDS, 30.8% died. Interleukin (IL)-6 was massively elevated at every time-point. The anti-inflammatory cytokine IL-10 was concomitantly upregulated with IL-6. The cellular response was characterized by lymphocytopenia with low counts of CD8+ T cells, natural killer (NK) and naïve T helper cells. CD8+ T and NK cells recovered after 8 to 14 days. The B cell system was largely unimpeded. This coincided with a slight increase in anti-SARS-CoV-2-Spike-RBD immunoglobulin (Ig) G and a decrease in anti-SARS-CoV-2-Spike-RBD IgM. GDF-15 levels were elevated throughout ICU treatment.
Massively elevated levels of IL-6 and a delayed cytotoxic immune defense characterized severe COVID-19-induced ARDS. The B cell response and antibody production were largely unimpeded. No obvious imbalance of pro- and anti-inflammatory mechanisms was observed, with elevated GDF-15 levels suggesting increased tissue resilience. |
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| AbstractList | The severity of Coronavirus Disease 2019 (COVID-19) is largely determined by the immune response. First studies indicate altered lymphocyte counts and function. However, interactions of pro- and anti-inflammatory mechanisms remain elusive. In the current study we characterized the immune responses in patients suffering from severe COVID-19-induced acute respiratory distress syndrome (ARDS).
This was a single-center retrospective study in patients admitted to the intensive care unit (ICU) with confirmed COVID-19 between March 14
and May 28
2020 (n = 39). Longitudinal data were collected within routine clinical care, including flow-cytometry of lymphocyte subsets, cytokine analysis and growth differentiation factor 15 (GDF-15). Antibody responses against the receptor binding domain (RBD) of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Spike protein were analyzed.
All patients suffered from severe ARDS, 30.8% died. Interleukin (IL)-6 was massively elevated at every time-point. The anti-inflammatory cytokine IL-10 was concomitantly upregulated with IL-6. The cellular response was characterized by lymphocytopenia with low counts of CD8+ T cells, natural killer (NK) and naïve T helper cells. CD8+ T and NK cells recovered after 8 to 14 days. The B cell system was largely unimpeded. This coincided with a slight increase in anti-SARS-CoV-2-Spike-RBD immunoglobulin (Ig) G and a decrease in anti-SARS-CoV-2-Spike-RBD IgM. GDF-15 levels were elevated throughout ICU treatment.
Massively elevated levels of IL-6 and a delayed cytotoxic immune defense characterized severe COVID-19-induced ARDS. The B cell response and antibody production were largely unimpeded. No obvious imbalance of pro- and anti-inflammatory mechanisms was observed, with elevated GDF-15 levels suggesting increased tissue resilience. The severity of Coronavirus Disease 2019 (COVID-19) is largely determined by the immune response. First studies indicate altered lymphocyte counts and function. However, interactions of pro- and anti-inflammatory mechanisms remain elusive. In the current study we characterized the immune responses in patients suffering from severe COVID-19-induced acute respiratory distress syndrome (ARDS).ObjectivesThe severity of Coronavirus Disease 2019 (COVID-19) is largely determined by the immune response. First studies indicate altered lymphocyte counts and function. However, interactions of pro- and anti-inflammatory mechanisms remain elusive. In the current study we characterized the immune responses in patients suffering from severe COVID-19-induced acute respiratory distress syndrome (ARDS).This was a single-center retrospective study in patients admitted to the intensive care unit (ICU) with confirmed COVID-19 between March 14th and May 28th 2020 (n = 39). Longitudinal data were collected within routine clinical care, including flow-cytometry of lymphocyte subsets, cytokine analysis and growth differentiation factor 15 (GDF-15). Antibody responses against the receptor binding domain (RBD) of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Spike protein were analyzed.MethodsThis was a single-center retrospective study in patients admitted to the intensive care unit (ICU) with confirmed COVID-19 between March 14th and May 28th 2020 (n = 39). Longitudinal data were collected within routine clinical care, including flow-cytometry of lymphocyte subsets, cytokine analysis and growth differentiation factor 15 (GDF-15). Antibody responses against the receptor binding domain (RBD) of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Spike protein were analyzed.All patients suffered from severe ARDS, 30.8% died. Interleukin (IL)-6 was massively elevated at every time-point. The anti-inflammatory cytokine IL-10 was concomitantly upregulated with IL-6. The cellular response was characterized by lymphocytopenia with low counts of CD8+ T cells, natural killer (NK) and naïve T helper cells. CD8+ T and NK cells recovered after 8 to 14 days. The B cell system was largely unimpeded. This coincided with a slight increase in anti-SARS-CoV-2-Spike-RBD immunoglobulin (Ig) G and a decrease in anti-SARS-CoV-2-Spike-RBD IgM. GDF-15 levels were elevated throughout ICU treatment.ResultsAll patients suffered from severe ARDS, 30.8% died. Interleukin (IL)-6 was massively elevated at every time-point. The anti-inflammatory cytokine IL-10 was concomitantly upregulated with IL-6. The cellular response was characterized by lymphocytopenia with low counts of CD8+ T cells, natural killer (NK) and naïve T helper cells. CD8+ T and NK cells recovered after 8 to 14 days. The B cell system was largely unimpeded. This coincided with a slight increase in anti-SARS-CoV-2-Spike-RBD immunoglobulin (Ig) G and a decrease in anti-SARS-CoV-2-Spike-RBD IgM. GDF-15 levels were elevated throughout ICU treatment.Massively elevated levels of IL-6 and a delayed cytotoxic immune defense characterized severe COVID-19-induced ARDS. The B cell response and antibody production were largely unimpeded. No obvious imbalance of pro- and anti-inflammatory mechanisms was observed, with elevated GDF-15 levels suggesting increased tissue resilience.ConclusionsMassively elevated levels of IL-6 and a delayed cytotoxic immune defense characterized severe COVID-19-induced ARDS. The B cell response and antibody production were largely unimpeded. No obvious imbalance of pro- and anti-inflammatory mechanisms was observed, with elevated GDF-15 levels suggesting increased tissue resilience. ObjectivesThe severity of Coronavirus Disease 2019 (COVID-19) is largely determined by the immune response. First studies indicate altered lymphocyte counts and function. However, interactions of pro- and anti-inflammatory mechanisms remain elusive. In the current study we characterized the immune responses in patients suffering from severe COVID-19-induced acute respiratory distress syndrome (ARDS).MethodsThis was a single-center retrospective study in patients admitted to the intensive care unit (ICU) with confirmed COVID-19 between March 14th and May 28th 2020 (n = 39). Longitudinal data were collected within routine clinical care, including flow-cytometry of lymphocyte subsets, cytokine analysis and growth differentiation factor 15 (GDF-15). Antibody responses against the receptor binding domain (RBD) of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Spike protein were analyzed.ResultsAll patients suffered from severe ARDS, 30.8% died. Interleukin (IL)-6 was massively elevated at every time-point. The anti-inflammatory cytokine IL-10 was concomitantly upregulated with IL-6. The cellular response was characterized by lymphocytopenia with low counts of CD8+ T cells, natural killer (NK) and naïve T helper cells. CD8+ T and NK cells recovered after 8 to 14 days. The B cell system was largely unimpeded. This coincided with a slight increase in anti-SARS-CoV-2-Spike-RBD immunoglobulin (Ig) G and a decrease in anti-SARS-CoV-2-Spike-RBD IgM. GDF-15 levels were elevated throughout ICU treatment.ConclusionsMassively elevated levels of IL-6 and a delayed cytotoxic immune defense characterized severe COVID-19-induced ARDS. The B cell response and antibody production were largely unimpeded. No obvious imbalance of pro- and anti-inflammatory mechanisms was observed, with elevated GDF-15 levels suggesting increased tissue resilience. |
| Author | Kranke, Peter Meybohm, Patrick Lotz, Christopher Wedekink, Florian Gernert, Michael Schmalzing, Marc Sorger, Lena Notz, Quirin Herrmann, Johannes Schlegel, Nicolas Schmid, Benedikt Sitter, Magdalena Schlesinger, Tobias Weismann, Dirk Wischhusen, Jörg |
| AuthorAffiliation | 4 Department of Internal Medicine I, University Hospital Würzburg , Würzburg , Germany 1 Department of Anesthesiology and Intensive Care Medicine, University Hospital Würzburg , Würzburg , Germany 5 Department of General, Visceral, Vascular and Pediatric Surgery (Surgery I), University Hospital Würzburg , Würzburg , Germany 3 Department of Gynecology, Section for Experimental Tumor Immunology, University Hospital Würzburg , Würzburg , Germany 2 Department of Medicine II, Rheumatology and Clinical Immunology, University Hospital Würzburg , Würzburg , Germany |
| AuthorAffiliation_xml | – name: 3 Department of Gynecology, Section for Experimental Tumor Immunology, University Hospital Würzburg , Würzburg , Germany – name: 2 Department of Medicine II, Rheumatology and Clinical Immunology, University Hospital Würzburg , Würzburg , Germany – name: 4 Department of Internal Medicine I, University Hospital Würzburg , Würzburg , Germany – name: 5 Department of General, Visceral, Vascular and Pediatric Surgery (Surgery I), University Hospital Würzburg , Würzburg , Germany – name: 1 Department of Anesthesiology and Intensive Care Medicine, University Hospital Würzburg , Würzburg , Germany |
| Author_xml | – sequence: 1 givenname: Quirin surname: Notz fullname: Notz, Quirin – sequence: 2 givenname: Marc surname: Schmalzing fullname: Schmalzing, Marc – sequence: 3 givenname: Florian surname: Wedekink fullname: Wedekink, Florian – sequence: 4 givenname: Tobias surname: Schlesinger fullname: Schlesinger, Tobias – sequence: 5 givenname: Michael surname: Gernert fullname: Gernert, Michael – sequence: 6 givenname: Johannes surname: Herrmann fullname: Herrmann, Johannes – sequence: 7 givenname: Lena surname: Sorger fullname: Sorger, Lena – sequence: 8 givenname: Dirk surname: Weismann fullname: Weismann, Dirk – sequence: 9 givenname: Benedikt surname: Schmid fullname: Schmid, Benedikt – sequence: 10 givenname: Magdalena surname: Sitter fullname: Sitter, Magdalena – sequence: 11 givenname: Nicolas surname: Schlegel fullname: Schlegel, Nicolas – sequence: 12 givenname: Peter surname: Kranke fullname: Kranke, Peter – sequence: 13 givenname: Jörg surname: Wischhusen fullname: Wischhusen, Jörg – sequence: 14 givenname: Patrick surname: Meybohm fullname: Meybohm, Patrick – sequence: 15 givenname: Christopher surname: Lotz fullname: Lotz, Christopher |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33123167$$D View this record in MEDLINE/PubMed |
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| Copyright | Copyright © 2020 Notz, Schmalzing, Wedekink, Schlesinger, Gernert, Herrmann, Sorger, Weismann, Schmid, Sitter, Schlegel, Kranke, Wischhusen, Meybohm and Lotz. Copyright © 2020 Notz, Schmalzing, Wedekink, Schlesinger, Gernert, Herrmann, Sorger, Weismann, Schmid, Sitter, Schlegel, Kranke, Wischhusen, Meybohm and Lotz 2020 Notz, Schmalzing, Wedekink, Schlesinger, Gernert, Herrmann, Sorger, Weismann, Schmid, Sitter, Schlegel, Kranke, Wischhusen, Meybohm and Lotz |
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| Keywords | Coronavirus Disease 2019 immune response inflammation Severe Acute Respiratory Syndrome Coronavirus 2 acute respiratory distress syndrome cytokines growth differentiation factor 15 |
| Language | English |
| License | Copyright © 2020 Notz, Schmalzing, Wedekink, Schlesinger, Gernert, Herrmann, Sorger, Weismann, Schmid, Sitter, Schlegel, Kranke, Wischhusen, Meybohm and Lotz. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 ObjectType-Undefined-3 This article was submitted to Inflammation, a section of the journal Frontiers in Immunology Edited by: Rudolf Lucas, Augusta University, United States Reviewed by: Juerg Hamacher, Lindenhofspital, Switzerland; Daniel Scott-Algara, Institut Pasteur, France |
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| SubjectTerms | acute respiratory distress syndrome Aged Antibodies, Viral - blood Antibodies, Viral - immunology Betacoronavirus - immunology Coronavirus Disease 2019 Coronavirus Infections - immunology Coronavirus Infections - pathology COVID-19 Cytokine Release Syndrome - immunology Cytokine Release Syndrome - pathology cytokines Female growth differentiation factor 15 Growth Differentiation Factor 15 - blood Humans Immunoglobulin G - blood Immunoglobulin G - immunology Immunology inflammation Intensive Care Units Interleukin-10 - blood Interleukin-6 - blood Longitudinal Studies Lymphopenia Male Middle Aged Pandemics Pilot Projects Pneumonia, Viral - immunology Pneumonia, Viral - pathology Retrospective Studies SARS-CoV-2 Severe Acute Respiratory Syndrome - immunology Severe Acute Respiratory Syndrome - pathology Severe Acute Respiratory Syndrome Coronavirus 2 Spike Glycoprotein, Coronavirus - immunology |
| Title | Pro- and Anti-Inflammatory Responses in Severe COVID-19-Induced Acute Respiratory Distress Syndrome—An Observational Pilot Study |
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