<HashMap><database>EGA</database><scores/><additional><omics_type>Genomics</omics_type><dataset_type>N/A</dataset_type><submitter_keywords>COVID-19</submitter_keywords><submitter_keywords>SARS-CoV-2</submitter_keywords><submitter_keywords>2019 novel coronavirus infection</submitter_keywords><submitter_keywords>2019-nCoV infection</submitter_keywords><submitter_keywords>severe acute respiratory syndrome coronavirus 2</submitter_keywords><submitter_keywords>coronavirus disease 2019</submitter_keywords><submitter_keywords>SARS-coronavirus 2</submitter_keywords><full_dataset_link>https://ega-archive.org/datasets/EGAD00001006828</full_dataset_link><sample_count>33</sample_count><description>EGA dataset EGAD00001006828</description><repository>EGA</repository><title>Hypertension delays viral clearance and exacerbates airway hyperinflammation in patients with COVID-19</title><pubmed_abstract>In coronavirus disease 2019 (COVID-19), hypertension and cardiovascular diseases are major risk factors for critical disease progression. However, the underlying causes and the effects of the main anti-hypertensive therapies-angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs)-remain unclear. Combining clinical data (n = 144) and single-cell sequencing data of airway samples (n = 48) with in vitro experiments, we observed a distinct inflammatory predisposition of immune cells in patients with hypertension that correlated with critical COVID-19 progression. ACEI treatment was associated with dampened COVID-19-related hyperinflammation and with increased cell intrinsic antiviral responses, whereas ARB treatment related to enhanced epithelial-immune cell interactions. Macrophages and neutrophils of patients with hypertension, in particular under ARB treatment, exhibited higher expression of the pro-inflammatory cytokines CCL3 and CCL4 and the chemokine receptor CCR1. Although the limited size of our cohort does not allow us to establish clinical efficacy, our data suggest that the clinical benefits of ACEI treatment in patients with COVID-19 who have hypertension warrant further investigation.</pubmed_abstract><pubmed_title>Hypertension delays viral clearance and exacerbates airway hyperinflammation in patients with COVID-19.</pubmed_title><pubmed_authors>Trump Saskia S, Lukassen Soeren S, Anker Markus S MS, Chua Robert Lorenz RL, Liebig Johannes J, Thürmann Loreen L, Corman Victor Max VM, Binder Marco M, Loske Jennifer J, Klasa Christina C, Krieger Teresa T, Hennig Bianca P BP, Messingschlager Marey M, Pott Fabian F, Kazmierski Julia J, Twardziok Sven S, Albrecht Jan Philipp JP, Eils Jürgen J, Hadzibegovic Sara S, Lena Alessia A, Heidecker Bettina B, Bürgel Thore T, Steinfeldt Jakob J, Goffinet Christine C, Kurth Florian F, Witzenrath Martin M, Völker Maria Theresa MT, Müller Sarah Dorothea SD, Liebert Uwe Gerd UG, Ishaque Naveed N, Kaderali Lars L, Sander Leif-Erik LE, Drosten Christian C, Laudi Sven S, Eils Roland R, Conrad Christian C, Landmesser Ulf U, Lehmann Irina I</pubmed_authors></additional><is_claimable>false</is_claimable><name>ena-DATASET-DKFZ-24-12-2020-10:12:59:494-197 - samples</name><description>In Coronavirus Disease 2019 (COVID-19), hypertension and cardiovascular diseases are major risk factors for critical disease
progression. However, the underlying reasons and the effect of the main anti-hypertensive therapiesÃ¢Â€Â”angiotensin-converting
enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs)Ã¢Â€Â”remain unclear. Combining clinical data (n = 144) and
single-cell sequencing data of airway samples (n = 48) with in vitro experiments, we observed a distinct inflammatory predisposition
of immune cells in patients with hypertension that correlated with critical disease progression. ACEI treatment
associated with dampened COVID-19-related hyperinflammation and with increased cell intrinsic anti-viral responses, whereas
ARB treatment related to enhanced epithelialÃ¢Â€Â“immune cell interactions. Macrophages and neutrophils of patients with hypertension,
in particular under ARB treatment, exhibited higher expression of the pro-inflammatory cytokines CCL3 and CCL4
and the chemokine receptor CCR1. Although the limited size of our cohort does not allow us to establish clinical efficacy, our
data suggest that the clinical benefits of ACEI treatment in patients with COVID-19 who have hypertension warrant further
investigation.</description><dates><updated>2021-02-16 08:02:27</updated></dates><accession>EGAD00001006828</accession><cross_references><TAXONOMY>9606</TAXONOMY><pubmed>33361824</pubmed><OLS>MONDO_0100096</OLS><EGA>EGAC00001001627</EGA><EGA>EGAS00001004772</EGA></cross_references></HashMap>