Inflammatory Markers and Cytokines in Moderate and Critical Cases of COVID-19

Chang, Soon Hee; Minn, Dohsik; Kim, Shin‐Woo; Kim, Yu Kyung

doi:10.7754/clin.lab.2021.210142

Cited by 13 publications

(14 citation statements)

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“…The main risk factors for severe and long COVID-19 include age, male sex, smoking, presence of comorbidities (obesity, diabetes, hypertension, heart disease) and variations in the immune response of the host ( Zhou et al., 2020 ; Ejaz et al., 2020 ; Wang et al., 2021; Chang et al., 2021 ). Evidence suggests that age is the most significant risk factor for the severe form of COVID-19 and related complications ( Chen et al., 2021 ).…”

Section: Discussionmentioning

confidence: 99%

“…The duration and severity of COVID-19 is related to several factors, including viral (mutations) ( Nagy et al., 2021 ) and host (age, sex, comorbidities and immunological) factors (Wang et al., 2021; Chang et al., 2021 ). SARS-CoV-2 infection begins with its binding to the ACE2 protein of alveolar epithelial cells, which induces activation of the innate and adaptive immune responses through the production and interaction of chemokines, colony-stimulating factors, interferons, interleukins, and tumor necrosis factor-α (TNF-α).…”

Section: Introductionmentioning

confidence: 99%

“…The term “cytokine storm” was coined to describe intense production of cytokines in infectious processes responsible for triggering immunopathological reactions ( Teijaro, 2017 ). Among the inflammatory mediators released by immune cells, the cytokines IFN-α, IFN-γ, IL-1β, IL-6, IL-12, IL-18, IL-33, TNF-α and TGF-β are highlighted, and altered levels are associated with different clinical features of COVID-19 ( Huang et al., 2021a ; Chang et al., 2021 ). Indeed, cytokine storms correlate with the severity and progression of COVID-19 and can result in serious complications such as acute respiratory distress syndrome (ARDS) and multiple organ failure, which are the leading causes of death from the disease ( Kunnumakkara et al., 2021 ).…”

Section: Introductionmentioning

confidence: 99%

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Cytokine Profiles Associated With Acute COVID-19 and Long COVID-19 Syndrome

Queiroz

Neves

Lima

et al. 2022

Front. Cell. Infect. Microbiol.

154

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The duration and severity of COVID-19 are related to age, comorbidities, and cytokine synthesis. This study evaluated the impact of these factors on patients with clinical presentations of COVID-19 in a Brazilian cohort. A total of 317 patients diagnosed with COVID-19 were included; cases were distributed according to clinical status as severe (n=91), moderate (n=56) and mild (n=170). Of these patients, 92 had acute COVID-19 at sample collection, 90 had already recovered from COVID-19 without sequelae, and 135 had sequelae (long COVID syndrome). In the acute COVID-19 group, patients with the severe form had higher IL-6 levels (p=0.0260). In the post-COVID-19 group, there was no significant difference in cytokine levels between groups with different clinical conditions. In the acute COVID-19 group, younger patients had higher levels of TNF-α, and patients without comorbidities had higher levels of TNF-α, IL-4 and IL-2 (p<0.05). In contrast, patients over age 60 with comorbidities had higher levels of IL-6. In the post-COVID-19 group, subjects with long COVID-19 had higher levels of IL-17 and IL-2 (p<0.05), and subjects without sequelae had higher levels of IL-10, IL-6 and IL- 4 (p<0.05). Our results suggest that advanced age, comorbidities and elevated serum IL-6 levels are associated with severe COVID-19 and are good markers to differentiate severe from mild cases. Furthermore, high serum levels of IL-17 and IL-2 and low levels of IL-4 and IL-10 appear to constitute a cytokine profile of long COVID-19, and these markers are potential targets for COVID-19 treatment and prevention strategies.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Cytokine Profiles Associated With Acute COVID-19 and Long COVID-19 Syndrome

Queiroz

Neves

Lima

et al. 2022

Front. Cell. Infect. Microbiol.

154

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“…Cytokines play a crucial role in the evolution of infections, both microbial and viral, and determine the duration and severity of infections. Particularly for COVID-19, the course and outcome of the disease are determined by viral (mutational) and host (e.g., age, sex, comorbidities, and immunological) factors [ 106 , 107 ]. In SARS-CoV-2 infection, the innate and adaptive immune systems are activated following binding of the virus to the angiotensin-converting enzyme 2 (ACE2) protein of alveolar epithelial cells and subsequent production and interaction of chemokines, colony-stimulating factors, interferons, interleukins, and TNF-a.…”

Section: Cytokine Release and Long-covidmentioning

confidence: 99%

“…When the immune response is dysregulated, it contributes to disease pathogenesis, as in the case of a “cytokine storm” [ 110 , 111 ], or hypercytokinemia, which is characterized by (a) perpetuated activation of lymphocytes and macrophages causing immune dysregulation, (b) large secretions of cytokines caused by such perpetuated activation, and (c) overwhelming systemic inflammation and multi-organ failure with high mortality [ 112 , 113 ]. The most important inflammatory mediators released by immune cells during the “cytokine storm” are IFN-α, IFN-γ, IL-1β, IL-6, IL-12, IL-18, IL-33, TNF-a, and TGF-β and they are associated with different clinical features of COVID-19 [ 106 , 114 ]. Indeed, cytokine storms correlate with the severity and progression of COVID-19 and can result in serious complications such as acute respiratory distress syndrome (ARDS) and multiple organ failure, which are the leading causes of death from the disease [ 115 , 116 ].…”

Section: Cytokine Release and Long-covidmentioning

confidence: 99%

New Insights into SARS-CoV-2 and Cancer Cross-Talk: Does a Novel Oncogenesis Driver Emerge?

et al. 2022

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Since the pandemic’s onset, a growing population of individuals has recovered from SARS-CoV-2 infection and its long-term effects in some of the convalescents are gradually being reported. Although the precise etiopathogenesis of post-acute COVID-19 sequelae (PACS) remains elusive, the mainly accepted rationale is that SARS-CoV-2 exerts long-lasting immunomodulatory effects, promotes chronic low-grade inflammation, and causes irreversible tissue damage. So far, several viruses have been causally linked to human oncogenesis, whereas chronic inflammation and immune escape are thought to be the leading oncogenic mechanisms. Excessive cytokine release, impaired T-cell responses, aberrant activation of regulatory signaling pathways (e.g., JAK-STAT, MAPK, NF-kB), and tissue damage, hallmarks of COVID-19 disease course, are also present in the tumor microenvironment. Therefore, the intersection of COVID-19 and cancer is partially recognized and the long-term effects of the virus on oncogenesis and cancer progression have not been explored yet. Herein, we present an up-to-date review of the current literature regarding COVID-19 and cancer cross-talk, as well as the oncogenic pathways stimulated by SARS-CoV-2.

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Could the fibromyalgia syndrome be triggered or enhanced by COVID-19?

Fialho

Oliveira

2023

Inflammopharmacol

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Fibromyalgia (FM) is a complex disease with an uncertain aetiology and intricate pathophysiology. Although its genesis is not fully explained, potential environmental factors, such as viral infections might trigger FM or worsen patients' clinical outcomes. The SARS-CoV-2 virus may affect central and peripheral nervous systems, leading to musculoskeletal, neurological, and psychological disturbances. These symptoms might persist at least 12 months beyond the recovery, often referred to as post-COVID syndrome, which resembles FM syndrome. In this sense, we argued the potential consequences of COVID-19 exclusively on FM syndrome. First, we have described post-COVID syndrome and its painful symptoms. Afterwards, we argued whether FM syndrome could be triggered or enhanced by COVID-19 infection or by numerous and persistent stressors imposed daily by the pandemic setting (isolation, uncertainty, depression, mental stress, generalized anxiety, and fear of the virus). In addition, we have demonstrated similarities between pathophysiological mechanisms and cardinal symptoms of FM and COVID-19, speculating that SARS-CoV-2 might represent a critical mediator of FM or an exacerbator of its symptoms once both syndromes share similar mechanisms and complaints. Therefore, pharmacologic and non-pharmacological approaches commonly used to treat FM could serve as strategic therapies to attenuate painful and neurological manifestations of post-COVID syndrome. Although it is still theoretical, clinicians and researchers should be alert of patients who develop symptoms similar to FM or those who had their FM symptoms increased post-COVID to manage them better. Graphical Abstract

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Inflammatory Markers and Cytokines in Moderate and Critical Cases of COVID-19

Cited by 13 publications

References 0 publications

Cytokine Profiles Associated With Acute COVID-19 and Long COVID-19 Syndrome

Cytokine Profiles Associated With Acute COVID-19 and Long COVID-19 Syndrome

New Insights into SARS-CoV-2 and Cancer Cross-Talk: Does a Novel Oncogenesis Driver Emerge?

Could the fibromyalgia syndrome be triggered or enhanced by COVID-19?

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