Monocytes and macrophages in severe COVID‐19 – friend, foe or both?

Dress, Regine J.; Ginhoux, Florent

doi:10.1111/imcb.12464

Cited by 11 publications

(13 citation statements)

References 16 publications

(31 reference statements)

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“…It has been revealed that CD163 + myeloid cells can be detected in damaged alveolar tissue of patients with COVID-19 [17] , [18] , [19] . Moreover, in a time-and-severity manner, lymphocyte frequency in blood circulation was reduced in patients with severe SARS-CoV-2 infection [20] . In contrast, the frequency of inflammatory HLA‐DR low CD163 high monocytes increased within the blood circulation, resulting in infiltration of these monocytes into the airways upon release of CCL2 by activated airway tissue-resident memory T cells [20] .…”

Section: Introductionmentioning

confidence: 94%

“…Moreover, in a time-and-severity manner, lymphocyte frequency in blood circulation was reduced in patients with severe SARS-CoV-2 infection [20] . In contrast, the frequency of inflammatory HLA‐DR low CD163 high monocytes increased within the blood circulation, resulting in infiltration of these monocytes into the airways upon release of CCL2 by activated airway tissue-resident memory T cells [20] . Furthermore, to confirm the importance of monocytes in the immunopathogenesis of COVID-19, high plasma levels of several inflammatory mediators, including CCL2, granulocyte–macrophage colony-stimulating factor (GM-CSF), CXCL8 (Interleukin-8), interferon gamma-induced protein 10 (IP-10), and osteopontin were detected in patients with SARS-CoV-2 infection [21] .…”

Section: Introductionmentioning

confidence: 94%

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Role of CCL2/CCR2 axis in the pathogenesis of COVID-19 and possible Treatments: All options on the Table

Ranjbar

Rahimi

Baghernejadan

et al. 2022

International Immunopharmacology

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Section: Introductionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 94%

Role of CCL2/CCR2 axis in the pathogenesis of COVID-19 and possible Treatments: All options on the Table

Ranjbar

Rahimi

Baghernejadan

et al. 2022

International Immunopharmacology

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“…However, it is also possible that the DNA methylation changes are partly due to the release of immature or altered monocytes from myelopoiesis, as reported for severe COVID-19 [93][94][95][96] and sepsis [63]. Release of immature myeloid cells from the bone marrow in severe COVID-19 is reminiscent of emergency myelopoiesis [97].…”

Section: Discussionmentioning

confidence: 96%

Epigenetic and transcriptomic reprogramming in monocytes of severe COVID-19 patients reflects alterations in myeloid differentiation and the influence of inflammatory cytokines

Godoy-Tena

Barmada

Morante-Palacios

et al. 2022

Preprint

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COVID-19 manifests with a wide spectrum of clinical phenotypes, ranging from asymptomatic and mild to severe and critical. Severe and critical COVID-19 patients are characterized by marked changes in the myeloid compartment, especially monocytes. However, little is known about the epigenetic alterations that occur in these cells during hyperinflammatory responses in severe COVID-19 patients. In this study, we obtained the DNA methylome and transcriptome of peripheral blood monocytes from severe COVID-19 patients. DNA samples extracted from CD14+CD15- monocytes of 48 severe COVID-19 patients and 11 healthy controls were hybridized on MethylationEPIC BeadChip arrays. In parallel, single-cell transcriptomics of 10 severe COVID-19 patients were generated. CellPhoneDB was used to infer changes in the crosstalk between monocytes and other immune cell types. We observed DNA methylation changes in CpG sites associated with interferon-related genes and genes associated with antigen presentation, concordant with gene expression changes. These changes significantly overlapped with those occurring in bacterial sepsis, although specific DNA methylation alterations in genes specific to viral infection were also identified. We also found these alterations to comprise some of the DNA methylation changes occurring during myeloid differentiation and under the influence of inflammatory cytokines. A progression of DNA methylation alterations in relation to the Sequential Organ Failure Assessment (SOFA) score was found to be related to interferon-related genes and T-helper 1 cell cytokine production. CellPhoneDB analysis of the single-cell transcriptomes of other immune cell types suggested the existence of altered crosstalk between monocytes and other cell types like NK cells and regulatory T cells. Our findings show the occurrence of an epigenetic and transcriptional reprogramming of peripheral blood monocytes, which could be associated with the release of aberrant immature monocytes, increased systemic levels of pro-inflammatory cytokines, and changes in immune cell crosstalk in these patients.

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“…While many groups rapidly delineated the cellular and soluble mediator profile of circulating blood from COVID-19 patients, it is clear that these peripheral abnormalities are not always reflective of the changes occurring within inflamed lung tissue ( Dress and Ginhoux, 2021 ). As described above, whole lung tissue is exceedingly challenging to acquire (especially out with autopsy sampling of fatal cases), whereas sampling of the airways via acquisition of bronchoalveolar lavage fluid (BALF) allows for analysis of luminal cells, with repeated sampling also possible.…”

Section: Macrophage As Mediators Of Organ Damage In Covid-19?mentioning

confidence: 99%