A combinational approach to restore cytokine balance and to inhibit virus growth may promote patient recovery in severe COVID-19 cases

Mahmud-Al-Rafat, Abdullah; Asim, Md. Muzammal Haque; Taylor‐Robinson, Andrew W.; Majumder, Apurba; Muktadir, Abdul; Muktadir, Hasneen; Karim, M.; Khan, Imran; Ahasan, M. M.; Billah, Morsaline

doi:10.1016/j.cyto.2020.155228

Cited by 9 publications

(5 citation statements)

References 96 publications

(126 reference statements)

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“…The binding of SARS-Cov2 to ACE2 receptor expressed on epithelial cells membrane of the respiratory tract, activates the pro-inflammatory cascade. ACE2 is a major regulator of the renin-angiotensin system (RAS) that acts by converting angiotensin (Ang) II to Ang 1–7, a key regulator of the blood pressure homeostasis and in the prevention of lung injury [ 60 ]. The Ang II hormone is vasoconstrictor that directly activates pro-inflammatory responses and the release of cytokines such as IL-6, IL-8 and TNFα by cells through NF-κβ up-regulation, whereas, the Ang 1–7 is a vasodilating hormone, responsible for the anti-inflammatory responses and thereby acting to prevent lungs damage.…”

Section: How Does Sars-cov-2 Initiate Cytokine Release and What Are Tmentioning

confidence: 99%

“…The ACE2 down-regulation is associated with RAS imbalance, increased pro-inflammatory response and multi-organ damage from SARS-CoV-2 infection. The mechanism of ACE2 shedding triggered by ADAM17 stimulation is not fully elucidated; however, lymphopenia and the presence of Ang II type 1 receptor (AT1R) are potent activators of such process [ 60 ] . In addition, SARS-CoV-2's association with pattern recognition receptors (PRRs) is instrumental in inducing cytokine, chemokine responses to build innate and adaptive immune responses.…”

Section: How Does Sars-cov-2 Initiate Cytokine Release and What Are Tmentioning

confidence: 99%

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The pro-inflammatory cytokines in COVID-19 pathogenesis: What goes wrong?

Darif

Hammi

Kihel

et al. 2021

Microbial Pathogenesis

237

195

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The outbreak of coronavirus disease 2019 (COVID-19), caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection, has emerged in China in December 2019 and rapidly spread to more than 196 countries worldwide. The physiopathology of human SARS-CoV-2 has not been completely understood, but its pathogenesis has been linked to a disproportionate response of the immune system. Just as described for SARS and MERS, an uncontrolled systemic inflammatory response, known as cytokine release syndrome (CRS) was observed in severe COVID-19 patients. It results from the release by immune and non-immune effector cells of substantial amounts of pro-inflammatory cytokines and appears to contribute to SARS-CoV-2 pulmonary inflammation and extensive lung damage. In addition, hyper-coagulation and thrombosis resulted from the important release of pro-inflammatory cytokines contribute to the lethality of subjects severely infected with SARS-CoV-2. It is therefore essential to have a deep understanding of the various cytokines involved in this exacerbated immune response, and that could be targeted by potential immunological treatments. The aim of this review was to gather the current knowledge about the role of pro-inflammatory cytokines, namely IL-1β, IL-6, IL-8, IL-17 and TNFα in SARS-CoV-2 CRS , the probable causes and clinical outcomes of this phenomenon in severe cases of COVID-19.

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Section: How Does Sars-cov-2 Initiate Cytokine Release and What Are Tmentioning

confidence: 99%

Section: How Does Sars-cov-2 Initiate Cytokine Release and What Are Tmentioning

confidence: 99%

The pro-inflammatory cytokines in COVID-19 pathogenesis: What goes wrong?

Darif

Hammi

Kihel

et al. 2021

Microbial Pathogenesis

237

195

View full text Add to dashboard Cite

show abstract

“…This would provide a further guide for clinical strategies to ameliorate the adverse effects of the infection i.e., the post-acute/long COVID-19 syndrome, in patients with or without COVID-19-mediated ischemic stroke. This is emphasized by the fact that cytokine restoration may interfere with and inhibit SARS-CoV-2 entry and infection, which in turn inhibits hyper-inflammation and hyper-coagulopathy [ 158 , 159 ]. Furthermore, this effort may also help to maintain the ACE2/Ang-(1-7)/MasR axis and reduce NLRP3 inflammasome activation, which would favor brain repair and secondary prevention efforts.…”

Section: Propositions and Future Prospectsmentioning

confidence: 99%

Neuroinflammation and COVID-19 Ischemic Stroke Recovery—Evolving Evidence for the Mediating Roles of the ACE2/Angiotensin-(1–7)/Mas Receptor Axis and NLRP3 Inflammasome

Nassir

Zolkefley

Ramli

et al. 2022

IJMS

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Cerebrovascular events, notably acute ischemic strokes (AIS), have been reported in the setting of novel coronavirus disease (COVID-19) infection. Commonly regarded as cryptogenic, to date, the etiology is thought to be multifactorial and remains obscure; it is linked either to a direct viral invasion or to an indirect virus-induced prothrombotic state, with or without the presence of conventional cerebrovascular risk factors. In addition, patients are at a greater risk of developing long-term negative sequelae, i.e., long-COVID-related neurological problems, when compared to non-COVID-19 stroke patients. Central to the underlying neurobiology of stroke recovery in the context of COVID-19 infection is reduced angiotensin-converting enzyme 2 (ACE2) expression, which is known to lead to thrombo-inflammation and ACE2/angiotensin-(1–7)/mitochondrial assembly receptor (MasR) (ACE2/Ang-(1-7)/MasR) axis inhibition. Moreover, after AIS, the activated nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) family pyrin domain-containing 3 (NLRP3) inflammasome may heighten the production of numerous proinflammatory cytokines, mediating neuro-glial cell dysfunction, ultimately leading to nerve-cell death. Therefore, potential neuroprotective therapies targeting the molecular mechanisms of the aforementioned mediators may help to inform rehabilitation strategies to improve brain reorganization (i.e., neuro-gliogenesis and synaptogenesis) and secondary prevention among AIS patients with or without COVID-19. Therefore, this narrative review aims to evaluate the mediating role of the ACE2/Ang- (1-7)/MasR axis and NLRP3 inflammasome in COVID-19-mediated AIS, as well as the prospects of these neuroinflammation mediators for brain repair and in secondary prevention strategies against AIS in stroke rehabilitation.

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“…In COVID-19 patients, several inflammatory markers are associated with neuropathogenesis. This immunologic phenomenon is called “cytokine storm”, characterized by the increase in pro-inflammatory cytokine levels leading to a systematic inflammation, exacerbating viral pathogenesis causing sepsis, ARDS, and multiorgan failure [ 106 , 107 , 108 , 109 , 110 ]. Such molecules signalize various immune cells such as white blood cells (B cells) or T cells to attack the virus.…”

Section: Mechanismmentioning

confidence: 99%

Neuropsychiatric Disorders and COVID-19: What We Know So Far

et al. 2021

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SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus-2) affects the central nervous system (CNS), which is shown in a significant number of patients with neurological events. In this study, an updated literature review was carried out regarding neurological disorders in COVID-19. Neurological symptoms are more common in patients with severe infection according to their respiratory status and divided into three categories: (1) CNS manifestations; (2) cranial and peripheral nervous system manifestations; and (3) skeletal muscle injury manifestations. Patients with pre-existing cerebrovascular disease are at a higher risk of admission to the intensive care unit (ICU) and mortality. The neurological manifestations associated with COVID-19 are of great importance, but when life-threatening abnormal vital signs occur in severely ill COVID-19 patients, neurological problems are usually not considered. It is crucial to search for new treatments for brain damage, as well as for alternative therapies that recover the damaged brain and reduce the inflammatory response and its consequences for other organs. In addition, there is a need to diagnose these manifestations as early as possible to limit long-term consequences. Therefore, much research is needed to explain the involvement of SARS-CoV-2 causing these neurological symptoms because scientists know zero about it.

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A combinational approach to restore cytokine balance and to inhibit virus growth may promote patient recovery in severe COVID-19 cases

Cited by 9 publications

References 96 publications

The pro-inflammatory cytokines in COVID-19 pathogenesis: What goes wrong?

The pro-inflammatory cytokines in COVID-19 pathogenesis: What goes wrong?

Neuroinflammation and COVID-19 Ischemic Stroke Recovery—Evolving Evidence for the Mediating Roles of the ACE2/Angiotensin-(1–7)/Mas Receptor Axis and NLRP3 Inflammasome

Neuropsychiatric Disorders and COVID-19: What We Know So Far

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