Respiratory and systemic monocytes, dendritic cells, and myeloid‐derived suppressor cells in COVID‐19: Implications for disease severity

Falck‐Jones, Sara; Österberg, Björn; Smed‐Sörensen, Anna

doi:10.1111/joim.13559

Cited by 19 publications

(13 citation statements)

References 121 publications

(306 reference statements)

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“…To gain insights into the type of cellular infiltrates present in the lungs over time post infection with BA.1, cellular deconvolution (SpacialDecon) analysis using full gene sets (S1 – S5 Tables) were used together with the gene expression matrices from the “Mouse Cell Atlas (MCA) Lung Cell expression matrix” and the “NanoString (NS) Immune Cell Family expression matrix”. As might be expected [74, 75], a series of innate mononuclear leukocyte populations were identified at 5 dpi, which included macrophages, monocytes, dendritic cells, and NK cells, as well as gamma delta T cells [76] (Fig. 3b).…”

Section: Resultssupporting

confidence: 52%

Tracking inflammation resolution signatures in lungs after SARS-CoV-2 omicron BA.1 infection of K18-hACE2 mice

Carolin,

Yan,

Bishop

et al. 2024

Preprint

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The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes Coronavirus Disease 2019 (COVID-19), which can result in severe disease often characterised by a 'cytokine storm' and the associated acute respiratory distress syndrome. However, many infections with SARS-CoV-2 are mild or asymptomatic throughout the course of infection. Although blood biomarkers of severe disease are well studied, less well understood are the inflammatory signatures in lung tissues associated with mild disease or silent infections, wherein infection and inflammation are rapidly resolved leading to sequelae-free recovery. Herein we described RNA-Seq and histological analyses of lungs over time in an omicron BA.1/K18-hACE2 mouse infection model, which displays these latter features. Although robust infection was evident at 2 days post infection (dpi), viral RNA was largely cleared by 10 dpi. Acute inflammatory signatures showed a slightly different pattern of cytokine signatures compared with severe infection models, but where much diminished 30 dpi and absent by 66 dpi. Cellular deconvolution identified significantly increased abundance scores for a number of anti-inflammatory pro-resolution cell types at 5/10 dpi. These included type II innate lymphoid cells, T regulatory cells, and interstitial macrophages. Genes whose expression trended downwards over 2 - 66 dpi included biomarkers of severe disease and were associated with 'cytokine storm' pathways. Genes whose expression trended upward during this period were associated with recovery of ciliated cells, AT2 to AT1 transition, reticular fibroblasts and innate lymphoid cells, indicating a return to homeostasis. Very few differentially expressed host genes were identified at 66 dpi, suggesting near complete recovery. The parallels between mild or subclinical infections in humans and those observed in this BA.1/K18-hACE2 mouse model are discussed.

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Section: Resultssupporting

confidence: 52%

Tracking inflammation resolution signatures in lungs after SARS-CoV-2 omicron BA.1 infection of K18-hACE2 mice

Carolin,

Yan,

Bishop

et al. 2024

Preprint

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“…A notable recent study (n = 19) examined these CD3 + CD4 + CD25 + CD127 low T cells up to 3 months after SARS-CoV-2 infection to find that IL-10 and TGF-β were produced upon stimulation with either S1 or N protein, and, importantly, that CD8 + cells were producing IFN-γ, as all 3 cytokines are required for suppression, proliferation, and anti-viral activity [ 385 ]. However, recently, studies on a novel cell type MDSCs, although not conclusive, are emerging to elucidate that, far from being clear, implicate TGF-β in COVID-19 MDSCs as suppressing CD4 + CD25 + Foxp3 + cells and evoking CD4 + CD25 − Foxp3 + expansion, affecting T REGS , the autoreactivity of T cells, and suppressing IFN-γ [ 187 , 386 ]. The differences between T FR and T REGS have been examined prior, in order to observe whether CD25 signaling is independent or dependent on IL-2.…”

Section: T Cells and The Adaptive Immune System In Sars-cov-2 Researchmentioning

confidence: 99%

Innate and Adaptive Immunity during SARS-CoV-2 Infection: Biomolecular Cellular Markers and Mechanisms

Brown¹,

Ojha²,

Fricke³

et al. 2023

Vaccines

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The coronavirus 2019 (COVID-19) pandemic was caused by a positive sense single-stranded RNA (ssRNA) severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). However, other human coronaviruses (hCoVs) exist. Historical pandemics include smallpox and influenza, with efficacious therapeutics utilized to reduce overall disease burden through effectively targeting a competent host immune system response. The immune system is composed of primary/secondary lymphoid structures with initially eight types of immune cell types, and many other subtypes, traversing cell membranes utilizing cell signaling cascades that contribute towards clearance of pathogenic proteins. Other proteins discussed include cluster of differentiation (CD) markers, major histocompatibility complexes (MHC), pleiotropic interleukins (IL), and chemokines (CXC). The historical concepts of host immunity are the innate and adaptive immune systems. The adaptive immune system is represented by T cells, B cells, and antibodies. The innate immune system is represented by macrophages, neutrophils, dendritic cells, and the complement system. Other viruses can affect and regulate cell cycle progression for example, in cancers that include human papillomavirus (HPV: cervical carcinoma), Epstein–Barr virus (EBV: lymphoma), Hepatitis B and C (HB/HC: hepatocellular carcinoma) and human T cell Leukemia Virus-1 (T cell leukemia). Bacterial infections also increase the risk of developing cancer (e.g., Helicobacter pylori). Viral and bacterial factors can cause both morbidity and mortality alongside being transmitted within clinical and community settings through affecting a host immune response. Therefore, it is appropriate to contextualize advances in single cell sequencing in conjunction with other laboratory techniques allowing insights into immune cell characterization. These developments offer improved clarity and understanding that overlap with autoimmune conditions that could be affected by innate B cells (B1+ or marginal zone cells) or adaptive T cell responses to SARS-CoV-2 infection and other pathologies. Thus, this review starts with an introduction into host respiratory infection before examining invaluable cellular messenger proteins and then individual immune cell markers.

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“…Wherever SARS-CoV-2 goes, it recruits a variety of immune cells, and later inducing the release of cytokines, including monocyte chemoattractant protein 1, granulocyte-macrophage colony-stimulating factor, macrophage colony-stimulating factor, interleukin-1 (IL-1), tumor necrosis factor α (TNF-α), and IL-6 (55)(56)(57)(58)(59)(60). As adipocytes swell to store excess energy, close interactions between adipocytes and host immune cells enhance lipolysis, resulting in abnormal adipocyte secretion (more leptin and less adiponectin), insulin resistance, and persistent low-level inflammation (61)(62)(63).…”

Section: Chronic Low-grade Inflammation Aggravates Tissue Damage and ...mentioning

confidence: 99%

The intersection of obesity and (long) COVID-19: Hypoxia, thrombotic inflammation, and vascular endothelial injury

Xiang

Jing

et al. 2023

Front. Cardiovasc. Med.

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The role of hypoxia, vascular endothelial injury, and thrombotic inflammation in worsening COVID-19 symptoms has been generally recognized. Damaged vascular endothelium plays a crucial role in forming in situ thrombosis, pulmonary dysfunction, and hypoxemia. Thrombotic inflammation can further aggravate local vascular endothelial injury and affect ventilation and blood flow ratio. According to the results of many studies, obesity is an independent risk factor for a variety of severe respiratory diseases and contributes to high mechanical ventilation rate, high mortality, and slow recovery in COVID-19 patients. This review will explore the mechanisms by which obesity may aggravate the acute phase of COVID-19 and delay long COVID recovery by affecting hypoxia, vascular endothelial injury, and thrombotic inflammation. A systematic search of PubMed database was conducted for papers published since January 2020, using the medical subject headings of “COVID-19” and “long COVID” combined with the following keywords: “obesity,” “thrombosis,” “endothelial injury,” “inflammation,” “hypoxia,” “treatment,” and “anticoagulation.” In patients with obesity, the accumulation of central fat restricts the expansion of alveoli, exacerbating the pulmonary dysfunction caused by SARS-CoV-2 invasion, inflammatory damage, and lung edema. Abnormal fat secretion and immune impairment further aggravate the original tissue damage and inflammation diffusion. Obesity weakens baseline vascular endothelium function leading to an early injury and pre-thrombotic state after infection. Enhanced procoagulant activity and microthrombi promote early obstruction of the vascular. Obesity also prolongs the duration of symptoms and increases the risk of sequelae after hospital discharge. Persistent viral presence, long-term inflammation, microclots, and hypoxia may contribute to the development of persistent symptoms, suggesting that patients with obesity are uniquely susceptible to long COVID. Early interventions, including supplemental oxygen, comprehensive antithrombotic therapy, and anti-inflammatory drugs, show effectiveness in many studies in the prevention of serious hypoxia, thromboembolic events, and systemic inflammation, and are therefore recommended to reduce intensive care unit admission, mortality, and sequelae.

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Respiratory and systemic monocytes, dendritic cells, and myeloid‐derived suppressor cells in COVID‐19: Implications for disease severity

Cited by 19 publications

References 121 publications

Tracking inflammation resolution signatures in lungs after SARS-CoV-2 omicron BA.1 infection of K18-hACE2 mice

Tracking inflammation resolution signatures in lungs after SARS-CoV-2 omicron BA.1 infection of K18-hACE2 mice

Innate and Adaptive Immunity during SARS-CoV-2 Infection: Biomolecular Cellular Markers and Mechanisms

The intersection of obesity and (long) COVID-19: Hypoxia, thrombotic inflammation, and vascular endothelial injury

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