Cytokine-induced liver injury in coronavirus disease-2019 (COVID-19): untangling the knots

Anirvan, Prajna; Narain, Sonali; Hajizadeh, Negin; Aloor, Fuad Zain; Singh, Shivaram Prasad

doi:10.1097/meg.0000000000002034

Cited by 15 publications

(16 citation statements)

References 117 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…TNF-α is a pyrogenic cytokine secreted by macrophages, monocytes, Th1 cells, Th17 cells, CD8 + T cells, and DCs during the acute phase of inflammation or infection ( 68 , 77 , 79 ). It is a central cytokine in viral diseases that increases vascular permeability ( 251 ) and is associated with several chronic inflammatory conditions and autoimmune diseases ( 68 ). For >20 years now, anti-TNF antibodies have been used for alleviating the severity of some autoimmune inflammatory diseases, including rheumatoid arthritis, inflammatory bowel disease, and ankylosing spondylitis.…”

Section: Cytokine Secretion Induced By Sars-cov-2 Infectionmentioning

confidence: 99%

“…GM-CSF further induces CD14 + CD16 + inflammatory monocytes to produce increased IL-6 ( 368 , 369 ). This could activate more macrophages and contribute to an inflammatory storm ( 251 , 368 , 369 ). This immune-mediated injury, accompanied by elevated concentrations of IL-1, IL-2, IL-10, and IFNγ, would lead to systemic inflammatory response syndrome (SIRS) ( 368 , 369 ).…”

Section: Clinical Symptomsmentioning

confidence: 99%

See 1 more Smart Citation

The Role of Cytokines and Chemokines in Severe Acute Respiratory Syndrome Coronavirus 2 Infections

Hsu

Peng

et al. 2022

Front. Immunol.

View full text Add to dashboard Cite

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has resulted in countless infections and caused millions of deaths since its emergence in 2019. Coronavirus disease 2019 (COVID-19)-associated mortality is caused by uncontrolled inflammation, aberrant immune response, cytokine storm, and an imbalanced hyperactive immune system. The cytokine storm further results in multiple organ failure and lung immunopathology. Therefore, any potential treatments should focus on the direct elimination of viral particles, prevention strategies, and mitigation of the imbalanced (hyperactive) immune system. This review focuses on cytokine secretions of innate and adaptive immune responses against COVID-19, including interleukins, interferons, tumor necrosis factor-alpha, and other chemokines. In addition to the review focus, we discuss potential immunotherapeutic approaches based on relevant pathophysiological features, the systemic immune response against SARS-CoV-2, and data from recent clinical trials and experiments on the COVID-19-associated cytokine storm. Prompt use of these cytokines as diagnostic markers and aggressive prevention and management of the cytokine storm can help determine COVID-19-associated morbidity and mortality. The prophylaxis and rapid management of the cytokine storm appear to significantly improve disease outcomes. For these reasons, this study aims to provide advanced information to facilitate innovative strategies to survive in the COVID-19 pandemic.

show abstract

Section: Cytokine Secretion Induced By Sars-cov-2 Infectionmentioning

confidence: 99%

Section: Clinical Symptomsmentioning

confidence: 99%

The Role of Cytokines and Chemokines in Severe Acute Respiratory Syndrome Coronavirus 2 Infections

Hsu

Peng

et al. 2022

Front. Immunol.

View full text Add to dashboard Cite

show abstract

“…The mechanism of liver injury in COVID-19 infection is postulated to be a result of direct cytopathic effects of the virus; immune imbalance and cytokine storm-related multiorgan damage; hypoxia-reperfusion dysfunction; and idiosyncratic, drug-induced liver injury due to medications used for the management of COVID-19 infection [30,31]. Early retrospective data from China and Italy showed that elevated inflammatory markers-particularly ferritin, CRP, LDH, interleukin 6 [IL-6], and D-dimer-were associated with severe illness and increased mortality [32].…”

Section: Discussionmentioning

confidence: 99%

“…Early retrospective data from China and Italy showed that elevated inflammatory markers-particularly ferritin, CRP, LDH, interleukin 6 [IL-6], and D-dimer-were associated with severe illness and increased mortality [32]. A severely dysregulated immune response to local inflammation (COVID-19-induced pneumonia) with heightened production of cytokines and chemokines that in turn act as chemoattractants for other inflammatory cells result in an exaggerated immune response with consequent systemic manifestations and multi-organ involvement [30]. This sequence of events, termed cytokine storm, has been shown to be a major determinant of poor survival in patients with COVID-19 infection [30].…”

Section: Discussionmentioning

confidence: 99%

“…A severely dysregulated immune response to local inflammation (COVID-19-induced pneumonia) with heightened production of cytokines and chemokines that in turn act as chemoattractants for other inflammatory cells result in an exaggerated immune response with consequent systemic manifestations and multi-organ involvement [30]. This sequence of events, termed cytokine storm, has been shown to be a major determinant of poor survival in patients with COVID-19 infection [30]. In a retrospective, single-center study of 148 COVID-19-infected patients, there were higher levels of procalcitonin and CRP in patients presenting with abnormal liver chemistries [33].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Risk factors and outcomes for acute-on-chronic liver failure in COVID-19: a large multi-center observational cohort study

et al. 2021

Self Cite

View full text Add to dashboard Cite

Objective Coronavirus disease 2019 [COVID-19] infection in patients with chronic liver disease [CLD] may precipitate acute-on-chronic liver failure [ACLF]. In a large multi-center cohort of COVID-19-infected patients, we aim to analyze (1) the outcomes of patients with underlying CLD [with and without cirrhosis] and (2) the development and impact of ACLF on in-hospital mortality. Design We identified 192 adults with CLD from among 10,859 patients with confirmed COVID-19 infection (admitted to any of 12 hospitals in a New York health care system between March 1, 2020 and April 27, 2020). ACLF was defined using the EASL-CLIF Consortium definition. Patient follow-up was through April 30, 2020, or until the date of discharge, transfer, or death. Results Of the 84 patients with cirrhosis, 32 [38%] developed ACLF, with respiratory failure [39%] and renal failure [26%] being the most common. Hispanic/Latino ethnicity was particularly at higher risk of in-hospital mortality [adjusted HR 4.92, 95% 1.27–19.09, p < 0.02] in cirrhosis despite having lower risk of development of ACLF [HR 0.26, 95% CI 0.08–0.89, p = 0.03]. Hypertension on admission predicted development of ACLF [HR 3.46, 95% CI 1.12–10.75, p = 0.03]. In-hospital mortality was not different between CLD patients with or without cirrhosis [ p = 0.24] but was higher in those with cirrhosis who developed ACLF [adjusted HR 9.06, 95% CI 2.63–31.12, p < 0.001] with a trend for increased mortality by grade of ACLF [ p = 0.002]. There was no difference in in-hospital mortality between the CLD cohort compared to matched control without CLD (log rank, p = 0.98) and between the cirrhosis cohort compared to matched control without cirrhosis (log rank, p = 0.51). Conclusion Development of ACLF is the main driver of increased in-hospital mortality in hospitalized patients with COVID-19 infection and cirrhosis. Supplementary Information The online version contains supplementary material available at 10.1007/s12072-021-10181-y.

show abstract

The roles of critical pro‐inflammatory cytokines in the drive of cytokine storm during SARS‐CoV‐2 infection

Qudus

Tian

Sirajuddin

et al. 2023

Journal of Medical Virology

View full text Add to dashboard Cite

In patients with severe COVID-19, acute respiratory distress syndrome (ARDS), multiple organ dysfunction syndrome (MODS), and even mortality can result from cytokine storm, which is a hyperinflammatory medical condition caused by the excessive and uncontrolled release of pro-inflammatory cytokines. High levels of numerous crucial pro-inflammatory cytokines, such as interleukin-1 (IL-1), IL-2, IL-6, tumor necrosis factor-α, interferon (IFN)-γ, IFN-induced protein 10 kDa, granulocyte-macrophage colony-stimulating factor, monocyte chemoattractant protein-1, and IL-10 and so on, have been found in severe COVID-19. They participate in cascade amplification pathways of pro-inflammatory responses through complex inflammatory networks. Here, we review the involvements of these critical inflammatory cytokines in SARS-CoV-2 infection and discuss their potential roles in triggering or regulating cytokine storm, which can help to understand the pathogenesis of severe COVID-19. So far, there is rarely effective therapeutic strategy for patients with cytokine storm besides using glucocorticoids, which is proved to result in fatal side effects. Clarifying the roles of key involved cytokines in the complex inflammatory network of cytokine storm will help to develop an ideal therapeutic intervention, such as neutralizing antibody of certain cytokine or inhibitor of some inflammatory signal pathways.

show abstract

Cytokine-induced liver injury in coronavirus disease-2019 (COVID-19): untangling the knots

Cited by 15 publications

References 117 publications

The Role of Cytokines and Chemokines in Severe Acute Respiratory Syndrome Coronavirus 2 Infections

The Role of Cytokines and Chemokines in Severe Acute Respiratory Syndrome Coronavirus 2 Infections

Risk factors and outcomes for acute-on-chronic liver failure in COVID-19: a large multi-center observational cohort study

The roles of critical pro‐inflammatory cytokines in the drive of cytokine storm during SARS‐CoV‐2 infection

Contact Info

Product

Resources

About