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SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE235437 | GEO | 2023/08/18

REPOSITORIES: GEO

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SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels.

Project description:Patients with coronavirus disease 2019 (COVID-19) present increased risk for ischemic cardiovascular complications up to 1 year after infection. Although the systemic inflammatory response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection likely contributes to this increased cardiovascular risk, whether SARS-CoV-2 directly infects the coronary vasculature and attendant atherosclerotic plaques remains unknown. Here we report that SARS-CoV-2 viral RNA is detectable and replicates in coronary lesions taken at autopsy from severe COVID-19 cases. SARS-CoV-2 targeted plaque macrophages and exhibited a stronger tropism for arterial lesions than adjacent perivascular fat, correlating with macrophage infiltration levels. SARS-CoV-2 entry was increased in cholesterol-loaded primary macrophages and dependent, in part, on neuropilin-1. SARS-CoV-2 induced a robust inflammatory response in cultured macrophages and human atherosclerotic vascular explants with secretion of cytokines known to trigger cardiovascular events. Our data establish that SARS-CoV-2 infects coronary vessels, inducing plaque inflammation that could trigger acute cardiovascular complications and increase the long-term cardiovascular risk.

| S-EPMC10702930 | biostudies-literature

SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary [plaque]

Project description:COVID-19 patients present higher risk for myocardial infarction (MI), acute coronary syndrome, and stroke for up to 1 year after SARS-CoV-2 infection. While the systemic inflammatory response to SARS-CoV-2 infection likely contributes to this increased cardiovascular risk, whether SARS35 CoV-2 directly infects the coronary vasculature and attendant atherosclerotic plaques to locally promote inflammation remains unknown. Here, we report that SARS-CoV-2 viral RNA (vRNA) is detectable and the virus replicates in coronary atherosclerotic lesions taken at autopsy from patients with severe COVID-19.

2023-08-18 | GSE235435 | GEO

SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary [scRNA-seq]

2023-08-18 | GSE235436 | GEO

SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary [MAC_FOAM-RNAseq]

2023-08-18 | GSE235433 | GEO

SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary

Project description:SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary

| PRJNA986061 | ENA

SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary [plaque]

Project description:SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary [plaque]

| PRJNA986067 | ENA

SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary [MAC_FOAM-RNAseq]

Project description:SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary [MAC_FOAM-RNAseq]

| PRJNA986066 | ENA

SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary [scRNA-seq]

Project description:SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary [scRNA-seq]

| PRJNA986069 | ENA

Control of complement-induced inflammatory responses to SARS-CoV-2 infection by anti-SARS-CoV-2 antibodies

Project description:Dysregulated immune responses contribute to the excessive and uncontrolled inflammation observed in severe COVID-19. However, how immunity to SARS-CoV-2 is induced and regulated remains unclear. Here we uncover a role of the complement system in the induction of innate and adaptive immunity to SARS-CoV-2. Complement rapidly opsonizes SARS-CoV-2 particles via the lectin pathway. Complement-opsonized SARS-CoV-2 efficiently induces type-I interferon and pro-inflammatory cytokine responses via activation of dendritic cells, which are inhibited by antibodies against the complement receptors (CR) 3 and 4. Serum from COVID-19 patients, or monoclonal antibodies against SARS-CoV-2, attenuate innate and adaptive immunity induced by complement-opsonized SARS-CoV-2. Blocking of CD32, the FcγRII antibody receptor of dendritic cells, restores complement-induced immunity. These results suggest that opsonization of SARS-CoV-2 by complement is involved in the induction of innate and adaptive immunity to SARS-CoV-2 in the acute phase of infection. Subsequent antibody responses limit inflammation and restore immune homeostasis. These findings suggest that dysregulation of the complement system and FcγRII signaling may contribute to severe COVID-19.

| S-SCDT-10_1038-S44318-024-00061-0 | biostudies-other

Neutrophil-epithelial interactions augment infectivity and pro-inflammatory responses to SARS-CoV-2 infection.

Project description:In response to viral infection, neutrophils release inflammatory mediators as part of the innate immune response, contributing to pathogen clearance through virus internalization and killing. Pre-existing co-morbidities, correlating to incidence of severe COVID-19, are associated with chronic airway neutrophilia and examination of COVID-19 lung tissue revealed a series of epithelial pathologies associated with infiltration and activation of neutrophils. To determine the impact of neutrophil-epithelial interactions on the infectivity and inflammatory response to SARS-CoV-2 infection, we developed a co-culture model of airway neutrophilia. We discovered that SARS-CoV-2 infection of the airway epithelium alone does not result in a notable release of pro-inflammatory cytokines, however in the presence of neutrophils, the inflammatory response is both polarized and significantly augmented, epithelial barrier integrity in impaired and viral load of the airway epithelium increased. This study reveals a key role for neutrophil-epithelial interactions in determining inflammation, infectivity, and outcomes in response to SARS-CoV-2 infection.HighlightsWe have developed a model to study neutrophil-epithelial interactions which better reflects the in vivo situation than monocultures Neutrophils significantly augment SARS-CoV-2 mediated, pro-inflammatory cytokine release from the epithelium indicating a key interactionSARS-CoV-2 infection leads to a polarized inflammatory response in differentiated airway epitheliumDisruption of the epithelial barrier via addition of neutrophils or cytokines leads to increased infectionStudy reveals a key role for neutrophil-epithelial interactions in determining outcome/infectivity.

| S-EPMC8366793 | biostudies-literature

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