Dataset Information

Elevated Level of Circulating but Not Urine S100A8/A9 Identifies Poor COVID-19 Outcomes.

ABSTRACT: The alarmin calprotectin (S100A8/A9) is thought to drive a cytokine storm, a hallmark of severe COVID-19. Recent studies report circulating S100A8/A9 levels can distinguish COVID-19 severity but have only been conducted in non-U.S. cohorts and mainly focus on serum S100A8/A9 levels. Thus, we quantified S100A8/A9 in serum and urine samples from a hospital cohort in St. Louis, Missouri, to expand the understanding of S100A8/A9 as a prognostic biomarker for COVID-19. Elevated S100A8/A9 serum levels were observed in ICU patients (n = 49, p = 0.0370) and patients with fatal cases of COVID-19 (n = 76, p = 0.0018). We observed no correlation in the S100A8/A9 levels in matched serum and urine samples. Our results support the association of serum S100A8/A9 levels with COVID-19 severity and suggest that further investigation of urine S100A8/A9 as a COVID-19 biomarker is not warranted.

SUBMITTER: Mellett L

PROVIDER: S-EPMC10580308 | biostudies-literature | 2023 Oct

REPOSITORIES: biostudies-literature

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Elevated Level of Circulating but Not Urine S100A8/A9 Identifies Poor COVID-19 Outcomes.

Mellett Leah L Amarasinghe Gaya G Farnsworth Christopher W CW Khader Shabaana A SA

ACS infectious diseases 20231003 10

The alarmin calprotectin (S100A8/A9) is thought to drive a cytokine storm, a hallmark of severe COVID-19. Recent studies report circulating S100A8/A9 levels can distinguish COVID-19 severity but have only been conducted in non-U.S. cohorts and mainly focus on serum S100A8/A9 levels. Thus, we quantified S100A8/A9 in serum and urine samples from a hospital cohort in St. Louis, Missouri, to expand the understanding of S100A8/A9 as a prognostic biomarker for COVID-19. Elevated S100A8/A9 serum levels ...[more]

PMID: 37787461

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Project description:BackgroundMyocardial infarction (MI) triggers myelopoiesis, resulting in heightened production of neutrophils. However, the mechanisms that sustain their production and recruitment to the injured heart are unclear.MethodsUsing a mouse model of the permanent ligation of the left anterior descending artery and flow cytometry, we first characterized the temporal and spatial effects of MI on different myeloid cell types. We next performed global transcriptome analysis of different cardiac cell types within the infarct to identify the drivers of the acute inflammatory response and the underlying signaling pathways. Using a combination of genetic and pharmacological strategies, we identified the sequelae of events that led to MI-induced myelopoiesis. Cardiac function was assessed by echocardiography. The association of early indexes of neutrophilia with major adverse cardiovascular events was studied in a cohort of patients with acute MI.ResultsInduction of MI results in rapid recruitment of neutrophils to the infarct, where they release specific alarmins, S100A8 and S100A9. These alarmins bind to the Toll-like receptor 4 and prime the nod-like receptor family pyrin domain-containing 3 inflammasome in naïve neutrophils and promote interleukin-1β secretion. The released interleukin-1β interacts with its receptor (interleukin 1 receptor type 1) on hematopoietic stem and progenitor cells in the bone marrow and stimulates granulopoiesis in a cell-autonomous manner. Genetic or pharmacological strategies aimed at disruption of S100A8/A9 and their downstream signaling cascade suppress MI-induced granulopoiesis and improve cardiac function. Furthermore, in patients with acute coronary syndrome, higher neutrophil count on admission and after revascularization correlates positively with major adverse cardiovascular disease outcomes.ConclusionsOur study provides novel evidence for the primary role of neutrophil-derived alarmins (S100A8/A9) in dictating the nature of the ensuing inflammatory response after myocardial injury. Therapeutic strategies aimed at disruption of S100A8/A9 signaling or their downstream mediators (eg, nod-like receptor family pyrin domain-containing 3 inflammasome, interleukin-1β) in neutrophils suppress granulopoiesis and may improve cardiac function in patients with acute coronary syndrome.

Dataset Information

Elevated Level of Circulating but Not Urine S100A8/A9 Identifies Poor COVID-19 Outcomes.

Publications

Elevated Level of Circulating but Not Urine S100A8/A9 Identifies Poor COVID-19 Outcomes.

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