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Pro- and Anti-Inflammatory Responses in Severe COVID-19-Induced Acute Respiratory Distress Syndrome—An Observational Pilot Study

Zitieren Sie bitte immer diese URN: urn:nbn:de:bvb:20-opus-212815
  • Objectives 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). Methods This was a single-center retrospective study in patients admitted to the intensive care unit (ICU) with confirmed COVID-19 betweenObjectives 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). Methods 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. Results 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. Conclusions 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.zeige mehrzeige weniger

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Autor(en): Quirin Notz, Marc Schmalzing, Florian Wedekink, Tobias Schlesinger, Michael Gernert, Johannes Herrmann, Lena Sorger, Dirk Weismann, Benedikt Schmid, Magdalena Sitter, Nicolas Schlegel, Peter Kranke, Jörg Wischhusen, Patrick MeybohmORCiD, Christopher Lotz
URN:urn:nbn:de:bvb:20-opus-212815
Dokumentart:Artikel / Aufsatz in einer Zeitschrift
Institute der Universität:Medizinische Fakultät / Klinik und Poliklinik für Allgemein-, Viszeral-, Gefäß- und Kinderchirurgie (Chirurgische Klinik I)
Medizinische Fakultät / Frauenklinik und Poliklinik
Medizinische Fakultät / Klinik und Poliklinik für Anästhesiologie (ab 2004)
Medizinische Fakultät / Medizinische Klinik und Poliklinik I
Medizinische Fakultät / Medizinische Klinik und Poliklinik II
Sprache der Veröffentlichung:Englisch
Titel des übergeordneten Werkes / der Zeitschrift (Englisch):Frontiers in Immunology
ISSN:1664-3224
Erscheinungsjahr:2020
Band / Jahrgang:11
Aufsatznummer:581338
Originalveröffentlichung / Quelle:Frontiers in Immunology 2020, 11:581338. doi: 10.3389/fimmu.2020.581338
DOI:https://doi.org/10.3389/fimmu.2020.581338
Allgemeine fachliche Zuordnung (DDC-Klassifikation):6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit / 610 Medizin und Gesundheit
Freie Schlagwort(e):Coronavirus Disease 2019; Severe Acute Respiratory Syndrome Coronavirus 2; acute respiratory distress syndrome; cytokines; growth differentiation factor 15; immune response; inflammation
Datum der Freischaltung:10.03.2021
Datum der Erstveröffentlichung:06.10.2020
Open-Access-Publikationsfonds / Förderzeitraum 2020
Lizenz (Deutsch):License LogoCC BY: Creative-Commons-Lizenz: Namensnennung 4.0 International