Illuminating the immunopathology of <scp>SARS‐CoV</scp>‐2

Saksena, Suraj; Chattopadhyay, Pratip K.

doi:10.1002/cyto.b.21988

Cited by 12 publications

(9 citation statements)

References 69 publications

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“…Moreover, SARS-CoV-2-specific CD4+ and CD8+ T cell responses are detected in recovered patients ( [54,55]. Several studies corroborated that lymphopenia occurs in COVID-19, which is associated with the extent of inflammation and disease severity [52]. Severe disease is characterized by significant dysregulation of the innate immune responses.…”

Section: The Host Immune Response To Sars-cov-2 Infectionmentioning

confidence: 94%

“…SARS-CoV-2 specifically binds via the spike glycoprotein in the crown structure, which leads to alteration in the viral wall envelope. This virus-human cell interaction triggers the release of numerous immune mediators, including cytokines and chemokines aimed at destroying the virus [52]. In this regard, the levels of CXCL10, IL-6 and IL-10 in the blood have been shown to be associated with outcome [53].…”

Section: The Host Immune Response To Sars-cov-2 Infectionmentioning

confidence: 99%

“…Hyperactivated T cells in severe disease also exhibit a trend toward cellular exhaustion. Pro-inflammatory responses such as increases in IL-6-or granulocytemacrophage colony-stimulating factor (GM-CSF)-producing CD4+ T cells in the blood and decreases in immunoregulatory regulatory T cells (Treg) or γδ T cells are further observations [52].…”

Section: The Host Immune Response To Sars-cov-2 Infectionmentioning

confidence: 99%

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Multiple Sclerosis and SARS-CoV-2 Vaccination: Considerations for Immune-Depleting Therapies

Sellner

2021

Vaccines

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Several concerns have been raised about the use of immunodepleting agents including alemtuzumab, cladribine and CD20-depleting antibodies in people with multiple sclerosis (pwMS) during the coronavirus disease (COVID) 2019 pandemic. As the end of the pandemic is not yet in sight, vaccination against severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) may be an elegant strategy to overcome the potential hazards associated with initiating and continuing treatment with immune-depleting agents. In this review, we summarize the immunological effects of immune-depleting therapy and underlying considerations for the hitherto existing recommendations that suggest a restricted use of immune-deleting therapies during the pandemic. Moreover, we critically discuss open questions regarding vaccination in general and against SARS-CoV-2 in pwMS.

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Section: The Host Immune Response To Sars-cov-2 Infectionmentioning

confidence: 94%

Section: The Host Immune Response To Sars-cov-2 Infectionmentioning

confidence: 99%

Section: The Host Immune Response To Sars-cov-2 Infectionmentioning

confidence: 99%

See 1 more Smart Citation

Multiple Sclerosis and SARS-CoV-2 Vaccination: Considerations for Immune-Depleting Therapies

Sellner

2021

Vaccines

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“…However, in COVID-19 patients with obesity, γδ T cells are negatively subjected to the combination of viral and host factors possibly. A decreased number of γδ T cells were found in COVID-19 cases 134 . In the inflammatory context induced by obesity, γδ T cells showed reduced number, impaired homeostasis and antiviral function in humans due to their high sensitivity to inflammation, leading to poor repair of lung lesions and worse pathological changes 81 .…”

Section: Dysfunctional Antiviral Immunity Induced By Obesity Fails To Eliminate Sars-cov-2 and Might Explain Severe Covid-19mentioning

confidence: 89%

Obesity and severe coronavirus disease 2019: molecular mechanisms, paths forward, and therapeutic opportunities

Yan¹,

Xiao²,

Wang³

et al. 2021

Theranostics

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) appears to have higher pathogenicity among patients with obesity. Obesity, termed as body mass index greater than 30 kg/m 2 , has now been demonstrated to be important comorbidity for disease severity during coronavirus disease 2019 (COVID-19) pandemic and associated with adverse events. Unraveling mechanisms behind this phenomenon can assist scientists, clinicians, and policymakers in responding appropriately to the COVID-19 pandemic. In this review, we systemically delineated the potential mechanistic links between obesity and worsening COVID-19 from altered physiology, underlying diseases, metabolism, immunity, cytokine storm, and thrombosis. Problematic ventilation caused by obesity and preexisting medical disorders exacerbate organ dysfunction for patients with obesity. Chronic metabolic disorders, including dyslipidemia, hyperglycemia, vitamin D deficiency, and polymorphisms of metabolism-related genes in obesity, probably aid SARS-CoV-2 intrusion and impair antiviral responses. Obesity-induced inadequate antiviral immunity (interferon, natural killer cells, invariant natural killer T cell, dendritic cell, T cells, B cell) at the early stage of SARS-CoV-2 infection leads to delayed viral elimination, increased viral load, and expedited viral mutation. Cytokine storm, with the defective antiviral immunity, probably contributes to tissue damage and pathological progression, resulting in severe symptoms and poor prognosis. The prothrombotic state, driven in large part by endothelial dysfunction, platelet hyperactivation, hypercoagulability, and impaired fibrinolysis in obesity, also increases the risk of severe COVID-19. These mechanisms in the susceptibility to severe condition also open the possibility for host-directed therapies in population with obesity. By bridging work done in these fields, researchers can gain a holistic view of the paths forward and therapeutic opportunities to break the vicious cycle of obesity and its devastating complications in the next emerging pandemic.

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“…The broad variety of putative mechanisms that propofol exerts on PMNs shows that further studies are warranted to reveal the pathways responsible for these mechanisms. In particular, the high mortality rates caused by exaggerated PMN activation in severe diseases, such as sepsis 48 or COVID-19, 49 , 50 demonstrate the urgent need for continued research in this field.…”

Section: Discussionmentioning

confidence: 99%

Propofol Ameliorates Exaggerated Human Neutrophil Activation in a LPS Sepsis Model

Bredthauer¹,

Geiger²,

Gruber³

et al. 2021

JIR

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Background Sepsis is a leading cause of morbidity and mortality worldwide. Many patients suffering from sepsis are treated on intensive care units and many of them require mechanical ventilation under sedation or general anesthesia. Propofol, a drug used for these purposes, is known to interact with polymorphonuclear granulocytes (PMNs). Therefore, the aim of this study was to investigate the influence of propofol on PMN functions after experimental Gram-negative induced sepsis using lipopolysaccharide (LPS) stimulation. Methods A total of 34 granulocyte-enriched samples were collected from healthy subjects. PMNs were isolated by density gradient centrifugation and incubated simultaneously with either 6 µg/mL or 60 µg/mL propofol, or none (control). Additionally, the experimental sepsis samples were incubated with either 40 pg/mL or 400 pg/mL LPS. Live cell imaging was conducted in order to observe granulocyte chemotactic migration, ROS production, and NETosis. Flow cytometry was used to analyze viability and antigen expression. Results Propofol led to significantly reduced PMN track length (p < 0.001) and track speed (p < 0.014) after LPS-induced sepsis in a dose-dependent manner. NETosis (p = 0.018) and ROS production (p = 0.039) were accelerated by propofol without LPS incubation, indicating improved immune function. Propofol also ameliorated LPS-induced increased NETosis and ROS-production. Antigen expression for CD11b, CD62l and CD66b was unaffected by propofol. Conclusion Propofol improves LPS-induced exaggerated PMN activation in an ex vivo model. Beneficial effects due to restored immune function in septic patients might be possible, but needs further investigation.

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Illuminating the immunopathology of SARS‐CoV‐2

Cited by 12 publications

References 69 publications

Multiple Sclerosis and SARS-CoV-2 Vaccination: Considerations for Immune-Depleting Therapies

Multiple Sclerosis and SARS-CoV-2 Vaccination: Considerations for Immune-Depleting Therapies

Obesity and severe coronavirus disease 2019: molecular mechanisms, paths forward, and therapeutic opportunities

Propofol Ameliorates Exaggerated Human Neutrophil Activation in a LPS Sepsis Model

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