Immunouniverse of SARS-CoV-2

Jimenez, D.; Arias, Marbel Torres

doi:10.1080/25785826.2022.2066251

Cited by 10 publications

(6 citation statements)

References 475 publications

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“…The study of immune response in critical COVID-19 patients is important for providing information on the pathophysiology of respiratory failure and death associated with SARS-CoV-2 infection, especially in patients who require mechanical ventilation, where mortality ranges from 25% to 34% [ 26 ]. There is ample evidence of immune system dysregulation in severe and critical COVID-19 cases [ 3 , 6 , 27 , 28 , 29 ]. However, few studies have focused on the evolution of pulmonary and systemic inflammation in critical patients who recover or die.…”

Section: Discussionmentioning

confidence: 99%

Compartmentalized Regulation of Pulmonary and Systemic Inflammation in Critical COVID-19 Patients

Santiago

Gonçalves-Pereira

Vieira

et al. 2023

Viruses

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Critical COVID-19 has been associated with altered patterns of cytokines. Distinct inflammatory processes in systemic and pulmonary sites have been reported, but studies comparing these two sites are still scarce. We aimed to evaluate the profile of pulmonary and systemic cytokines and chemokines in critically ill COVID-19 patients. Levels of cytokines and chemokines were measured in plasma samples and minibronchoalveolar lavage of critical COVID-19 patients within 48 h and 5–8 days after intubation. Distinct inflammatory processes were observed in the lungs and blood, which were regulated separately. Survivor patients showed higher lung cytokine levels including IFN-γ, IL-2, IL-4, G-CSF, and CCL4, while nonsurvivors displayed higher levels in the blood, which included IL-6, CXCL8, CXCL10, CCL2, and CCL4. Furthermore, our findings indicate that high TNF and CXCL8 levels in the mini-BAL were associated with better lung oxygen exchange capacity, whereas high levels of IFN-γ in plasma were associated with worse lung function, as measured using the PaO2/FiO2 ratio. These results suggest that a robust and localized inflammatory response in the lungs is protective and associated with survival, whereas a systemic inflammatory response is detrimental and associated with mortality in critical COVID-19.

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Section: Discussionmentioning

confidence: 99%

Compartmentalized Regulation of Pulmonary and Systemic Inflammation in Critical COVID-19 Patients

Santiago

Gonçalves-Pereira

Vieira

et al. 2023

Viruses

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“…It is the seventh CoV identified to be infecting humans. The other CoVs identified are less pathogenic HCoV-HKU1, HCoV-NL63, HCoVOC43 and HCoV-229E, which cause mild upper respiratory tract infections leading to common colds and highly pathogenic middle eastern respiratory syndrome (MERS)-CoV and SARS-CoV that causes severe respiratory tract infections [2] , [3] . Initially, the lack of knowledge about the interaction of SARS-CoV-2 with the host significantly hampered the development of therapeutics.…”

Section: Introductionmentioning

confidence: 99%

Involvement of epigenetics in affecting host immunity during SARS-CoV-2 infection

Behura

Naik

Patel

et al. 2023

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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“…Clinically, COVID-19 is highly variable, commonly ranging from an asymptomatic to a mild course. However, in a significant percentage of patients, the disease has a severe course that progresses to acute respiratory distress syndrome (ARDS) and multiple organ dysfunction syndrome, due to an alteration of the inflammatory and immune response, known as “cytokine storm” [ 1 ]. To enter the host cells, SARS-CoV-2 recognizes ACE2 (Angiotensin-converting enzyme 2) receptor and, subsequently, the serine protease TMPRSS2 is involved in the S protein priming [ 2 ].…”

Section: Introductionmentioning

confidence: 99%

“…ACE2 is localized in lipid rafts, small membrane microdomains enriched in cholesterol and glycosphingolipids, which are fundamental components in the entry and pathogenesis of the coronaviruses [ 3 ]. ACE2 receptor is expressed in different tissues and organs including colon, heart, brain, kidneys, and lungs, and its wide distribution could explain the multi-organ failure triggered by SARS-CoV-2 infection [ 1 ]. Once internalized through a mechanism that involves lipid rafts-dependent endocytosis [ 3 ], SARS-CoV-2 triggers the simultaneous activation of multiple receptors that culminates in uncontrolled and generalized inflammatory response, with an abnormal recruitment of immune cells and production of cytotoxic molecules.…”

Section: Introductionmentioning

confidence: 99%

“…Once internalized through a mechanism that involves lipid rafts-dependent endocytosis [ 3 ], SARS-CoV-2 triggers the simultaneous activation of multiple receptors that culminates in uncontrolled and generalized inflammatory response, with an abnormal recruitment of immune cells and production of cytotoxic molecules. The overblown production of pro-inflammatory mediators, amplifying the inflammation process, translates into serious tissues damage, ARDS, and cardiovascular complications [ 1 ].…”

Section: Introductionmentioning

confidence: 99%

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In Vitro Evidence of Statins’ Protective Role against COVID-19 Hallmarks

et al. 2022

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Despite the progressions in COVID-19 understanding, the optimization of patient-specific therapies remains a challenge. Statins, the most widely prescribed lipid-lowering drugs, received considerable attention due to their pleiotropic effects, encompassing lipid metabolism control and immunomodulatory and anti-thrombotic effects. In COVID-19 patients, statins improve clinical outcomes, reducing Intensive Care Unit admission, the onset of ARDS, and in-hospital death. However, the safety of statins in COVID-19 patients has been debated, mainly for statins’ ability to induce the expression of the ACE2 receptor, the main entry route of SARS-CoV-2. Unfortunately, the dynamic of statins’ mechanism in COVID-19 disease and prevention remains elusive. Using different in vitro models expressing different levels of ACE2 receptor, we investigated the role of lipophilic and hydrophilic statins on ACE2 receptor expression and subcellular localization. We demonstrated that the statin-mediated increase of ACE2 receptor expression does not necessarily coincide with its localization in lipid rafts domains, particularly after treatments with the lipophilic atorvastatin that disrupt lipid rafts’ integrity. Through a proteomic array, we analyzed the cytokine patterns demonstrating that statins inhibit the release of cytokines and factors involved in mild to severe COVID-19 cases. The results obtained provide additional information to dissect the mechanism underlying the protective effects of statin use in COVID-19.

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Immunouniverse of SARS-CoV-2

Cited by 10 publications

References 475 publications

Compartmentalized Regulation of Pulmonary and Systemic Inflammation in Critical COVID-19 Patients

Compartmentalized Regulation of Pulmonary and Systemic Inflammation in Critical COVID-19 Patients

Involvement of epigenetics in affecting host immunity during SARS-CoV-2 infection

In Vitro Evidence of Statins’ Protective Role against COVID-19 Hallmarks

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