Increased expression of hypoxia-induced factor 1α mRNA and its related genes in myeloid blood cells from critically ill COVID-19 patients

Taniguchi‐Ponciano, Keiko; Vadillo, Eduardo; Mayani, Héctor; González-Bonilla, César; Torres, Javier; Majluf, Abraham; Flores‐Padilla, Guillermo; Wacher, Niels H.; Galán, Juan Carlos; Ferat‐Osorio, Eduardo; Blanco-Favéla, Francisco; López-Macı́as, Constantino; Ferreira‐Hermosillo, Aldo; Ramírez‐Rentería, Claudia; Peña-Martínez, Eduardo; Silva-Román, Gloria; Vela-Patiño, Sandra; Mata-Lozano, Carlos; Carvente-Garcia, Roberto; Basurto-Acevedo, Lourdes; Saucedo, Renata; Piña‐Sánchez, Patricia; Chávez‐González, Antonieta; Marrero‐Rodríguez, Daniel; Mercado, Moisés

doi:10.1080/07853890.2020.1858234

Cited by 49 publications

(39 citation statements)

References 47 publications

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“…We found that HIF1A is increased in CD16+ monocytes in severe COVID-19 cases compared to healthy controls. This is consistent with another scRNAseq study that reported an increase in HIF1A in total monocytes in people with COVID-19 ( 42 ). Cytosolic accumulation of HIF-1α can lead to the switch in immune cell use of oxidative phosphorylation to aerobic glycolysis.…”

Section: Discussionsupporting

confidence: 93%

“…In addition, we found that CD16+ monocytes from people with severe COVID-19 had upregulated CXCL8 receptor genes, CXCR1 and CXCR2 , compared to mild cases. HIF-1α can induce upregulation of these three proteins, and hypoxia and viral infections have been shown to upregulate CXCL8 in monocytes ( 42 ). These findings suggest that upregulation of CXCL8 and its receptors, and other cytokine genes in CD16+ monocytes from severe COVID-19 amplify the inflammatory response of these cells, which may contribute to disease severity.…”

Section: Discussionmentioning

confidence: 99%

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Transcriptional Changes in CD16+ Monocytes May Contribute to the Pathogenesis of COVID-19

et al. 2021

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The COVID-19 pandemic has caused more than three million deaths globally. The severity of the disease is characterized, in part, by a dysregulated immune response. CD16+ monocytes are innate immune cells involved in inflammatory responses to viral infections, and tissue repair, among other functions. We characterized the transcriptional changes in CD16+ monocytes from PBMC of people with COVID-19, and from healthy individuals using publicly available single cell RNA sequencing data. CD16+ monocytes from people with COVID-19 compared to those from healthy individuals expressed transcriptional changes indicative of increased cell activation, and induction of a migratory phenotype. We also analyzed COVID-19 cases based on severity of the disease and found that mild cases were characterized by upregulation of interferon response and MHC class II related genes, whereas the severe cases had dysregulated expression of mitochondrial and antigen presentation genes, and upregulated inflammatory, cell movement, and apoptotic gene signatures. These results suggest that CD16+ monocytes in people with COVID-19 contribute to a dysregulated host response characterized by decreased antigen presentation, and an elevated inflammatory response with increased monocytic infiltration into tissues. Our results show that there are transcriptomic changes in CD16+ monocytes that may impact the functions of these cells, contributing to the pathogenesis and severity of COVID-19.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Transcriptional Changes in CD16+ Monocytes May Contribute to the Pathogenesis of COVID-19

et al. 2021

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“…The up-regulation and participation of HIF1alpha in events such as inflammation and immunometabolism make it a potential biomarker of COVID-19 severity. HIF1alpha and its transcriptionally regulated genes are also expressed in lung cells from severe COVID-19 patients, which may partially explain the hypoxia related events (64).…”

Section: Mdscs As Potential Biomarker In Covid-19mentioning

confidence: 97%

“…Immature myeloid subsets and bronchoalveolar cells of critically-ill COVID-19 patients have been found to express HIF1alpha, a critical regulator of the differentiation and function of MDSCs, and transcriptional targets related to inflammation (CXCL8, CXCR1, CXCR2, and CXCR4); virus sensing, (TLRs); and metabolism (SLC2A3, PFKFB3, PGK1, GAPDH and SOD2) (64). The up-regulation and participation of HIF1alpha in events such as inflammation and immunometabolism make it a potential biomarker of COVID-19 severity.…”

Section: Mdscs As Potential Biomarker In Covid-19mentioning

confidence: 99%

Myeloid-Derived Suppressor Cells as a Potential Biomarker and Therapeutic Target in COVID-19

Rowlands¹,

Segal²,

Hartl

2021

Front. Immunol.

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Clinical presentations of COVID-19 are highly variable, yet the precise mechanisms that govern the pathophysiology of different disease courses remain poorly defined. Across the spectrum of disease severity, COVID-19 impairs both innate and adaptive host immune responses by activating innate immune cell recruitment, while resulting in low lymphocyte counts. Recently, several reports have shown that patients with severe COVID-19 exhibit a dysregulated myeloid cell compartment, with increased myeloid-derived suppressor cells (MDSCs) correlating with disease severity. MDSCs, in turn, promote virus survival by suppressing T-cell responses and driving a highly pro-inflammatory state through the secretion of various mediators of immune activation. Here, we summarize the evidence on MDSCs and myeloid cell dysregulation in COVID-19 infection and discuss the potential of MDSCs as biomarkers and therapeutic targets in COVID-19 pneumonia and associated disease.

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“…Oalveolar cells, and participated in processes such as inflammation and immunometabolism, which make it a potential molecular marker for COVID-19 severity and molecular therapy [ 36 ]. Our research promoted CXCR4 as a biological target that could simplify detection methods.…”

Section: Discussionmentioning

confidence: 99%

Construction of an autophagy interaction network based on competitive endogenous RNA reveals the key pathways and central genes of SARS-CoV-2 infection in vivo

Chen

Wang

et al. 2021

Microbial Pathogenesis

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As of April 1, 2021, more than 2.8 million people have died of SARS-CoV-2 infection. In addition, the mutation of virus strains that have accompanied the pandemic has brought more severe challenges to pandemic control. Host microRNAs (miRNAs) are widely involved in a variety of biological processes of coronavirus infection, including autophagy in SARS-CoV-2 infection. However, the mechanisms underlying miRNAs involved in autophagy in SARS-CoV-2 infection have not been fully elucidated. In this study, the miRNA and messenger RNA (mRNA) expression profiles of patients with SARS-CoV-2 infection were investigated based on raw data from Gene Expression Omnibus (GEO) datasets, and potential novel biomarkers of autophagy were revealed by bioinformatics analyses. We identified 32 differentially expressed miRNAs and 332 differentially expressed mRNAs in patients with SARS-CoV-2 infection. Cytokine receptor related pathways were the most enriched pathways for differentially expressed miRNAs identified by pathway analysis. Most importantly, an autophagy interaction network, which was associated with the pathological processes of SARS-CoV-2 infection, especially with the cytokine storm, was constructed. In this network, hsa-miR-340–3p, hsa-miR-652–3p, hsa-miR-4772–5p, hsa-miR-192–5p, TP53INP2, and CCR2 may be biomarkers that predict changes in mild SARS-CoV-2 infection. Some molecules, including hsa-miR-1291 and CXCR4, were considered potential targets to predict the emergence of severe symptoms in SARS-CoV-2 infection. To our knowledge, this study provided the first profile analysis of an autophagy interaction network in SARS-CoV-2 infection and revealed several novel autophagy-related biomarkers for understanding the pathogenesis of SARS-CoV-2 infection in vivo.

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Increased expression of hypoxia-induced factor 1α mRNA and its related genes in myeloid blood cells from critically ill COVID-19 patients

Cited by 49 publications

References 47 publications

Transcriptional Changes in CD16+ Monocytes May Contribute to the Pathogenesis of COVID-19

Transcriptional Changes in CD16+ Monocytes May Contribute to the Pathogenesis of COVID-19

Myeloid-Derived Suppressor Cells as a Potential Biomarker and Therapeutic Target in COVID-19

Construction of an autophagy interaction network based on competitive endogenous RNA reveals the key pathways and central genes of SARS-CoV-2 infection in vivo

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