Bianca P Hennig

TL;DR: The data suggest that pharmacologic inhibition of the CCR1 and/or CCR5 pathways might suppress immune hyperactivation in critical COVID-19, which likely contribute to clinical observations of heightened inflammatory tissue damage, lung injury and respiratory failure.

TL;DR: This work investigates ACE2 and TMPRSS2 expression levels and their distribution across cell types in lung tissue and in cells derived from subsegmental bronchial branches by single nuclei and single cell RNA sequencing, suggesting increased vulnerability for SARS‐CoV‐2 infection.

TL;DR: In this paper, the authors observed a distinct inflammatory predisposition of immune cells in patients with hypertension that correlated with critical coronavirus disease 2019 (COVID-19)-related hyperinflammation and increased cell intrinsic antiviral responses, whereas ARB treatment related to enhanced epithelial-immune cell interactions.

TL;DR: This work investigates ACE2 and TMPRSS2 expression levels and their distribution across cell types in lung tissue and in cells derived from subsegmental bronchial branches by single nuclei and single cell RNA sequencing, suggesting increased vulnerability for SARS-CoV-2 infection.

TL;DR: This study provides novel insights into the pathophysiology of CO VID-19 and suggests an immunomodulatory therapy along the CCL2, CCL3/CCR1 axis as promising option to prevent and treat critical course of COVID-19.