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1.
Biochem Pharmacol ; 193: 114812, 2021 11.
Article in English | MEDLINE | ID: covidwho-1474355

ABSTRACT

Pulmonary fibrosis (PF) is characterised by several grades of chronic inflammation and collagen deposition in the interalveolar space and is a hallmark of interstitial lung diseases (ILDs). Recently, infectious agents have emerged as driving causes for PF development; however, the role of viral/bacterial infections in the initiation and propagation of PF is still debated. In this context, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus responsible for the current coronavirus disease 2019 (COVID-19) pandemic, has been associated with acute respiratory distress syndrome (ARDS) and PF development. Although the infection by SARS-CoV-2 can be eradicated in most cases, the development of fibrotic lesions cannot be precluded; furthermore, whether these lesions are stable or progressive fibrotic events is still unknown. Herein, an overview of the main molecular mechanisms driving the fibrotic process together with the currently approved and newly proposed therapeutic solutions was given. Then, the most recent data that emerged from post-COVID-19 patients was discussed, in order to compare PF and COVID-19-dependent PF, highlighting shared and specific mechanisms. A better understanding of PF aetiology is certainly needed, also to develop effective therapeutic strategies and COVID-19 pathology is offering one more chance to do it. Overall, the work reported here could help to define new approaches for therapeutic intervention in the diversity of the ILD spectrum.


Subject(s)
COVID-19/complications , Pulmonary Fibrosis/immunology , Pulmonary Fibrosis/metabolism , Animals , COVID-19/etiology , COVID-19/immunology , COVID-19/metabolism , Humans , Inflammation Mediators/immunology , Inflammation Mediators/metabolism , Neutrophils/immunology , Neutrophils/metabolism , Pulmonary Fibrosis/etiology
2.
Naunyn Schmiedebergs Arch Pharmacol ; 394(12): 2471-2474, 2021 12.
Article in English | MEDLINE | ID: covidwho-1473989

ABSTRACT

The pathophysiological process of the disease, Covid-19, is mediated by innate immunity, with the presence of macrophages responsible for secreting type 1 and 6 interleukins (IL), tumor necrosis factor (TNF) leading to dilation of endothelial cells with a consequent increase in capillary permeability. The treatment of this disease has been much discussed, but the variability in the clinical picture, the difficulties for diagnosis and treatment, especially of those patients who have the most severe clinical condition of the disease. Immunization is an effective tool for controlling the spread and overload of health services, but its effectiveness involves high investments in the acquisition of inputs, development of vaccines, and logistics of storage and distribution. These factors can be obstacles for countries with lower economic, technological, and infrastructure indexes. Reflecting on these difficulties, we raised the possibility of adjuvant therapies with imminent research feasibility, as is the case with the use of carvacrol, a monoterpenic phenol whose has biological properties that serve as a barrier to processes mediated by free radicals, such as irritation and inflammation, due to its antioxidant action. Many authors highlighted the activity of carvacrol as a potent suppressor of COX-2 expression minimizing the acute inflammatory process, decreasing the release of some pro-inflammatory mediators such as IL-1ß, TNF-α, PGE2. Anyway, the benefits of carvacrol are numerous and the therapeutic possibilities too. With this description, the question arises: would carvacrol be a supporting treatment option, effective in minimizing the deleterious effects of Covid-19? There is still a lot to discover and research.


Subject(s)
Antioxidants/therapeutic use , COVID-19/drug therapy , COVID-19/metabolism , Cymenes/therapeutic use , Animals , Anti-Infective Agents/pharmacology , Anti-Infective Agents/therapeutic use , Anti-Inflammatory Agents/pharmacology , Anti-Inflammatory Agents/therapeutic use , Antioxidants/pharmacology , COVID-19/immunology , Cymenes/pharmacology , Cytokine Release Syndrome/drug therapy , Cytokine Release Syndrome/immunology , Cytokine Release Syndrome/metabolism , Humans , Inflammation Mediators/antagonists & inhibitors , Inflammation Mediators/immunology , Inflammation Mediators/metabolism
3.
J Neuroinflammation ; 18(1): 231, 2021 Oct 13.
Article in English | MEDLINE | ID: covidwho-1468067

ABSTRACT

It is well accepted that environmental stressors experienced over a one's life, from microbial infections to chemical toxicants to even psychological stressors, ultimately shape central nervous system (CNS) functioning but can also contribute to its eventual breakdown. The severity, timing and type of such environmental "hits", woven together with genetic factors, likely determine what CNS outcomes become apparent. This focused review assesses the current COVID-19 pandemic through the lens of a multi-hit framework and disuses how the SARS-COV-2 virus (causative agent) might impact the brain and potentially interact with other environmental insults. What the long-term consequences of SAR2 COV-2 upon neuronal processes is yet unclear, but emerging evidence is suggesting the possibility of microglial or other inflammatory factors as potentially contributing to neurodegenerative illnesses. Finally, it is critical to consider the impact of the virus in the context of the substantial psychosocial stress that has been associated with the global pandemic. Indeed, the loneliness, fear to the future and loss of social support alone has exerted a massive impact upon individuals, especially the vulnerable very young and the elderly. The substantial upswing in depression, anxiety and eating disorders is evidence of this and in the years to come, this might be matched by a similar spike in dementia, as well as motor and cognitive neurodegenerative diseases.


Subject(s)
COVID-19/immunology , Inflammation Mediators/immunology , Mental Disorders/immunology , Neurodegenerative Diseases/immunology , Neuroimmunomodulation/immunology , Animals , Brain/immunology , COVID-19/epidemiology , Humans , Immunotherapy/trends , Mental Disorders/epidemiology , Mental Disorders/therapy , Neurodegenerative Diseases/epidemiology , Neurodegenerative Diseases/therapy , Stress, Psychological/epidemiology , Stress, Psychological/immunology , Stress, Psychological/therapy
6.
CNS Neurosci Ther ; 27(1): 36-47, 2021 01.
Article in English | MEDLINE | ID: covidwho-1388231

ABSTRACT

The blood-brain barrier (BBB) is an important physiological barrier that separates the central nervous system (CNS) from the peripheral circulation, which contains inflammatory mediators and immune cells. The BBB regulates cellular and molecular exchange between the blood vessels and brain parenchyma. Normal functioning of the BBB is crucial for the homeostasis and proper function of the brain. It has been demonstrated that peripheral inflammation can disrupt the BBB by various pathways, resulting in different CNS diseases. Recently, clinical research also showed CNS complications following SARS-CoV-2 infection and chimeric antigen receptor (CAR)-T cell therapy, which both lead to a cytokine storm in the circulation. Therefore, elucidation of the mechanisms underlying the BBB disruption induced by peripheral inflammation will provide an important basis for protecting the CNS in the context of exacerbated peripheral inflammatory diseases. In the present review, we first summarize the physiological properties of the BBB that makes the CNS an immune-privileged organ. We then discuss the relevance of peripheral inflammation-induced BBB disruption to various CNS diseases. Finally, we elaborate various factors and mechanisms of peripheral inflammation that disrupt the BBB.


Subject(s)
Blood-Brain Barrier/metabolism , Brain/metabolism , COVID-19/metabolism , Inflammation Mediators/metabolism , Animals , Blood-Brain Barrier/immunology , Blood-Brain Barrier/pathology , Brain/immunology , Brain/pathology , COVID-19/immunology , COVID-19/pathology , Endothelial Cells/immunology , Endothelial Cells/metabolism , Humans , Inflammation/immunology , Inflammation/metabolism , Inflammation/pathology , Inflammation Mediators/immunology
7.
Int J Med Sci ; 18(3): 846-851, 2021.
Article in English | MEDLINE | ID: covidwho-1389719

ABSTRACT

In the last 50 years we have experienced two big pandemics, the HIV pandemic and the pandemic caused by SARS-CoV-2. Both pandemics are caused by RNA viruses and have reached us from animals. These two viruses are different in the transmission mode and in the symptoms they generate. However, they have important similarities: the fear in the population, increase in proinflammatory cytokines that generate intestinal microbiota modifications or NETosis production by polymorphonuclear neutrophils, among others. They have been implicated in the clinical, prognostic and therapeutic attitudes.


Subject(s)
COVID-19/epidemiology , HIV Infections/epidemiology , HIV-1/pathogenicity , Pandemics/history , SARS-CoV-2/pathogenicity , COVID-19/immunology , COVID-19/psychology , COVID-19/transmission , Cytokines/blood , Cytokines/immunology , Extracellular Traps/immunology , Extracellular Traps/metabolism , Fear , Global Burden of Disease/statistics & numerical data , HIV Infections/immunology , HIV Infections/psychology , HIV Infections/transmission , HIV-1/immunology , HIV-1/isolation & purification , History, 20th Century , History, 21st Century , Host-Pathogen Interactions/immunology , Humans , Inflammation Mediators/blood , Inflammation Mediators/immunology , Mortality , Neutrophils/immunology , Neutrophils/metabolism , Pandemics/statistics & numerical data , Prognosis , SARS-CoV-2/immunology , SARS-CoV-2/isolation & purification
8.
Front Immunol ; 12: 720192, 2021.
Article in English | MEDLINE | ID: covidwho-1378190

ABSTRACT

COVID-19 might lead to multi-organ failure and, in some cases, to death. The COVID-19 severity is associated with a "cytokine storm." Danger-associated molecular patterns (DAMPs) are proinflammatory molecules that can activate pattern recognition receptors, such as toll-like receptors (TLRs). DAMPs and TLRs have not received much attention in COVID-19 but can explain some of the gender-, weight- and age-dependent effects. In females and males, TLRs are differentially expressed, likely contributing to higher COVID-19 severity in males. DAMPs and cytokines associated with COVID-19 mortality are elevated in obese and elderly individuals, which might explain the higher risk for severer COVID-19 in these groups. Adenosine signaling inhibits the TLR/NF-κB pathway and, through this, decreases inflammation and DAMPs' effects. As vaccines will not be effective in all susceptible individuals and as new vaccine-resistant SARS-CoV-2 mutants might develop, it remains mandatory to find means to dampen COVID-19 disease severity, especially in high-risk groups. We propose that the regulation of DAMPs via adenosine signaling enhancement might be an effective way to lower the severity of COVID-19 and prevent multiple organ failure in the absence of severe side effects.


Subject(s)
Alarmins/immunology , COVID-19/physiopathology , Inflammation Mediators/immunology , Adenosine/metabolism , Alarmins/antagonists & inhibitors , Animals , COVID-19/complications , COVID-19/immunology , COVID-19/therapy , Humans , Inflammation/prevention & control , Inflammation Mediators/antagonists & inhibitors , Multiple Organ Failure/etiology , Multiple Organ Failure/prevention & control , Patient Acuity , Signal Transduction , Toll-Like Receptors/antagonists & inhibitors , Toll-Like Receptors/immunology
10.
Biomed Pharmacother ; 141: 111794, 2021 Sep.
Article in English | MEDLINE | ID: covidwho-1263229

ABSTRACT

Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV2) is the causative agent of Corona Virus Disease 2019 (COVID-19). Lower production of type I and III interferons and higher levels of inflammatory mediators upon SARS-CoV2 infection contribute to COVID-19 pathogenesis. Optimal interferon production and controlled inflammation are essential to limit COVID-19 pathogenesis. However, the aggravated inflammatory response observed in COVID-19 patients causes severe damage to the host and frequently advances to acute respiratory distress syndrome (ARDS). Toll-like receptor 7 and 8 (TLR7/8) signaling pathways play a central role in regulating induction of interferons (IFNs) and inflammatory mediators in dendritic cells. Controlled inflammation is possible through regulation of TLR mediated response without influencing interferon production to reduce COVID-19 pathogenesis. This review focuses on inflammatory mediators that contribute to pathogenic effects and the role of TLR pathways in the induction of interferon and inflammatory mediators and their contribution to COVID-19 pathogenesis. We conclude that potential TLR7/8 agonists inducing antiviral interferon response and controlling inflammation are important therapeutic options to effectively eliminate SARS-CoV2 induced pathogenesis. Ongoing and future studies may provide additional evidence on their safety and efficacy to treat COVID-19 pathogenesis.


Subject(s)
COVID-19/metabolism , Inflammation Mediators/metabolism , Interferons/metabolism , Signal Transduction/physiology , Toll-Like Receptor 7/physiology , Toll-Like Receptor 8/physiology , Anti-Inflammatory Agents/administration & dosage , COVID-19/immunology , COVID-19/therapy , Humans , Inflammation Mediators/immunology , Interferons/immunology , Toll-Like Receptor 7/agonists , Toll-Like Receptor 8/agonists
13.
Biochem Biophys Res Commun ; 556: 87-92, 2021 06 04.
Article in English | MEDLINE | ID: covidwho-1173393

ABSTRACT

Virus-induced cytokine storm has been a devastating actuality in clinic. The abnormal production of type I interferon (IFN-1) and upregulation of multiple cytokines induced strong inflammation and thus lead to shock and organ failure. As an E3 ubiquitin ligase, tripartite motif-containing 37 (TRIM37) regulates the ubiquitination of multiple proteins including TRAFs. RNA sequencing was performed to investigated the alteration of transcriptional profile of H1N1-infected patients. qRT-PCR assay was performed to investigate the RNA levels of certain genes. The group of immune cells was examined by the Flow cytometry analysis. H&E staining was applied to evaluate lung inflammation of WT and TRIM37-KO mice. ELISA assay was performed to demonstrate the alteration of multiple cytokines. The protein levels in NF-kB signaling was estimated by western blotting and immunoprecipitation assays were applied to demonstrate the direct interaction between TRIM37 and TRAF-6. The RNA level of TRIM37 decreased in CD11b+ cells of Flu-infected patients. Knockout of TRIM37 inhibited the immune responses of H1N1-infected mice. TRIM37 deficiency reduced the levels of virous proinflammatory cytokines in bone marrow derived macrophages (BMDMs). Mechanically, TRIM37 promoted the K63-linked ubiquitination of TRAF6. TRIM37 negatively regulated inflammatory responses induced by virus infection via promoting TRAF6 ubiquitination at K63.


Subject(s)
Inflammation/metabolism , Orthomyxoviridae Infections/metabolism , Orthomyxoviridae Infections/virology , TNF Receptor-Associated Factor 6/metabolism , Tripartite Motif Proteins/metabolism , Ubiquitin-Protein Ligases/metabolism , Ubiquitination , Animals , Female , Humans , Inflammation Mediators/antagonists & inhibitors , Inflammation Mediators/immunology , Influenza A Virus, H1N1 Subtype/immunology , Influenza, Human/genetics , Influenza, Human/immunology , Influenza, Human/metabolism , Influenza, Human/virology , Mice , Mice, Inbred C57BL , Orthomyxoviridae Infections/genetics , Orthomyxoviridae Infections/immunology , TNF Receptor-Associated Factor 6/chemistry , Tripartite Motif Proteins/deficiency , Tripartite Motif Proteins/genetics , Ubiquitin-Protein Ligases/deficiency , Ubiquitin-Protein Ligases/genetics
14.
Inflammopharmacology ; 29(4): 939-963, 2021 Aug.
Article in English | MEDLINE | ID: covidwho-1169006

ABSTRACT

Coronavirus disease 2019 (COVID-19) is caused by the novel SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) first discovered in Wuhan, Hubei province, China in December 2019. SARS-CoV-2 has infected several millions of people, resulting in a huge socioeconomic cost and over 2.5 million deaths worldwide. Though the pathogenesis of COVID-19 is not fully understood, data have consistently shown that SARS-CoV-2 mainly affects the respiratory and gastrointestinal tracts. Nevertheless, accumulating evidence has implicated the central nervous system in the pathogenesis of SARS-CoV-2 infection. Unfortunately, however, the mechanisms of SARS-CoV-2 induced impairment of the central nervous system are not completely known. Here, we review the literature on possible neuropathogenic mechanisms of SARS-CoV-2 induced cerebral damage. The results suggest that downregulation of angiotensin converting enzyme 2 (ACE2) with increased activity of the transmembrane protease serine 2 (TMPRSS2) and cathepsin L in SARS-CoV-2 neuroinvasion may result in upregulation of proinflammatory mediators and reactive species that trigger neuroinflammatory response and blood brain barrier disruption. Furthermore, dysregulation of hormone and neurotransmitter signalling may constitute a fundamental mechanism involved in the neuropathogenic sequelae of SARS-CoV-2 infection. The viral RNA or antigenic peptides also activate or interact with molecular signalling pathways mediated by pattern recognition receptors (e.g., toll-like receptors), nuclear factor kappa B, Janus kinase/signal transducer and activator of transcription, complement cascades, and cell suicide molecules. Potential molecular targets and therapeutics of SARS-CoV-2 induced neurologic damage are also discussed.


Subject(s)
Blood-Brain Barrier/metabolism , Brain/metabolism , COVID-19/metabolism , Inflammation Mediators/metabolism , SARS-CoV-2/metabolism , Blood-Brain Barrier/immunology , Blood-Brain Barrier/pathology , Brain/immunology , Brain/pathology , COVID-19/immunology , COVID-19/pathology , Cytokine Release Syndrome/immunology , Cytokine Release Syndrome/metabolism , Cytokine Release Syndrome/pathology , Humans , Inflammation Mediators/immunology , SARS-CoV-2/immunology , Signal Transduction/physiology
15.
Pharmacol Res ; 168: 105581, 2021 06.
Article in English | MEDLINE | ID: covidwho-1157664

ABSTRACT

In-depth characterization of heart-brain communication in critically ill patients with severe acute respiratory failure is attracting significant interest in the COronaVIrus Disease 19 (COVID-19) pandemic era during intensive care unit (ICU) stay and after ICU or hospital discharge. Emerging research has provided new insights into pathogenic role of the deregulation of the heart-brain axis (HBA), a bidirectional flow of information, in leading to severe multiorgan disease syndrome (MODS) in patients with confirmed infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Noteworthy, HBA dysfunction may worsen the outcome of the COVID-19 patients. In this review, we discuss the critical role HBA plays in both promoting and limiting MODS in COVID-19. We also highlight the role of HBA as new target for novel therapeutic strategies in COVID-19 in order to open new translational frontiers of care. This is a translational perspective from the Italian Society of Cardiovascular Researches.


Subject(s)
Brain Diseases/therapy , Brain/drug effects , COVID-19/therapy , Heart Diseases/therapy , Heart/drug effects , Adrenal Cortex Hormones/administration & dosage , Anti-Inflammatory Agents/administration & dosage , Antiviral Agents/administration & dosage , Brain/immunology , Brain/metabolism , Brain Diseases/immunology , Brain Diseases/metabolism , COVID-19/immunology , COVID-19/metabolism , Critical Care/methods , Critical Illness/therapy , Dietary Supplements , Functional Food , Heart Diseases/immunology , Heart Diseases/metabolism , Humans , Inflammation Mediators/antagonists & inhibitors , Inflammation Mediators/immunology , Inflammation Mediators/metabolism , Microvessels/drug effects , Microvessels/immunology , Microvessels/metabolism , Multiple Organ Failure/immunology , Multiple Organ Failure/metabolism , Multiple Organ Failure/therapy , SARS-CoV-2/drug effects , SARS-CoV-2/immunology , SARS-CoV-2/metabolism
16.
J Immunol ; 206(7): 1597-1608, 2021 04 01.
Article in English | MEDLINE | ID: covidwho-1082059

ABSTRACT

Coronavirus disease 2019 (COVID-19) is associated with immune dysregulation and cytokine storm. Exploring the immune-inflammatory characteristics of COVID-19 patients is essential to reveal pathogenesis and predict progression. In this study, COVID-19 patients showed decreased CD3+, CD4+, and CD8+ T cells but increased neutrophils in circulation, exhibiting upregulated neutrophil-to-lymphocyte and neutrophil-to-CD8+ T cell ratio. IL-6, TNF-α, IL-1ß, IL-18, IL-12/IL-23p40, IL-10, Tim-3, IL-8, neutrophil extracellular trap-related proteinase 3, and S100A8/A9 were elevated, whereas IFN-γ and C-type lectin domain family 9 member A (clec9A) were decreased in COVID-19 patients compared with healthy controls. When compared with influenza patients, the expressions of TNF-α, IL-18, IL-12/IL-23p40, IL-8, S100A8/A9 and Tim-3 were significantly increased in critical COVID-19 patients, and carcinoembryonic Ag, IL-8, and S100A8/A9 could serve as clinically available hematologic indexes for identifying COVID-19 from influenza. Moreover, IL-6, IL-8, IL-1ß, TNF-α, proteinase 3, and S100A8/A9 were increased in bronchoalveolar lavage fluid of severe/critical patients compared with moderate patients, despite decreased CD4+ T cells, CD8+ T cells, B cells, and NK cells. Interestingly, bronchoalveolar IL-6, carcinoembryonic Ag, IL-8, S100A8/A9, and proteinase 3 were found to be predictive of COVID-19 severity and may serve as potential biomarkers for predicting COVID-19 progression and potential targets in therapeutic intervention of COVID-19.


Subject(s)
COVID-19 , Inflammation Mediators , SARS-CoV-2 , Severity of Illness Index , Aged , COVID-19/blood , COVID-19/immunology , Calgranulin A/blood , Calgranulin A/immunology , Calgranulin B/blood , Calgranulin B/immunology , Cytokines/blood , Cytokines/immunology , Disease Progression , Female , Hepatitis A Virus Cellular Receptor 2/blood , Hepatitis A Virus Cellular Receptor 2/immunology , Humans , Inflammation Mediators/blood , Inflammation Mediators/immunology , Leukocyte Count , Male , Middle Aged , Myeloblastin/blood , Myeloblastin/immunology , Retrospective Studies , SARS-CoV-2/immunology , SARS-CoV-2/metabolism
17.
J Infect Dis ; 223(3): 403-408, 2021 02 13.
Article in English | MEDLINE | ID: covidwho-1082007

ABSTRACT

We performed a retrospective study of coronavirus disease 2019 (COVID-19) in people with human immunodeficiency virus (PWH). PWH with COVID-19 demonstrated severe lymphopenia and decreased CD4+ T cell counts. Levels of inflammatory markers, including C-reactive protein, fibrinogen, D-dimer, interleukin 6, interleukin 8, and tumor necrosis factor α were commonly elevated. In all, 19 of 72 hospitalized individuals (26.4%) died and 53 (73.6%) recovered. PWH who died had higher levels of inflammatory markers and more severe lymphopenia than those who recovered. These findings suggest that PWH remain at risk for severe manifestations of COVID-19 despite antiretroviral therapy and that those with increased markers of inflammation and immune dysregulation are at risk for worse outcomes.


Subject(s)
COVID-19/immunology , COVID-19/virology , HIV Infections/immunology , HIV Infections/virology , Aged , COVID-19/blood , COVID-19/mortality , Female , HIV Infections/blood , HIV Infections/mortality , HIV-1/isolation & purification , Hospitalization/statistics & numerical data , Humans , Inflammation/blood , Inflammation/immunology , Inflammation/virology , Inflammation Mediators/blood , Inflammation Mediators/immunology , Lymphocyte Count , Lymphopenia/virology , Male , Middle Aged , New York/epidemiology , Retrospective Studies , Risk Factors , SARS-CoV-2/isolation & purification
19.
Arch Dermatol Res ; 314(1): 1-15, 2022 Jan.
Article in English | MEDLINE | ID: covidwho-1070839

ABSTRACT

We present the first reported cases of delayed inflammatory reactions (DIR) to hyaluronic acid (HA) dermal fillers after exposure to the COVID-19 spike protein. DIR to HA is reported to occur in the different scenarios including: secondary to poor injection technique, following dental cleaning procedures, following bacterial/viral illness, and after vaccination. In this report of 4 cases with distinct clinical histories and presentations: one case occured following a community acquired COVID-19 infection, one case occured in a study subject in the mRNA-1273 clinical phase III trial, one case occurred following the first dose of publically available mRNA-1273 vaccine (Moderna, Cambridge MA), and the last case occurred after the second dose of BNT162b2 vaccine (Pfizer, New York, NY). Injectable HA dermal fillers are prevalent in aesthetic medicine for facial rejuvenation. Structural modifications in the crosslinking of HA fillers have enhanced the products' resistance to enzymatic breakdown and thus increased injected product longevity, however, have also led to a rise in DIR. Previous, DIR to HA dermal fillers can present clinically as edema with symptomatic and inflammatory erythematous papules and nodules. The mechanism of action for the delayed reaction to HA fillers is unknown and is likely to be multifactorial in nature. A potential mechanism of DIR to HA fillers in COVID-19 related cases is binding and blockade of angiotensin 2 converting enzyme receptors (ACE2), which are targeted by the SARS-CoV-2 virus spike protein to gain entry into the cell. Spike protein interaction with dermal ACE2 receptors favors a pro-inflammatory, loco-regional TH1 cascade, promoting a CD8+T cell mediated reaction to incipient granulomas, which previously formed around residual HA particles. Management to suppress the inflammatory response in the native COVID-19 case required high-dose corticosteroids (CS) to suppress inflammatory pathways, with concurrent ACE2 upregulation, along with high-dose intralesional hyaluronidase to dissolve the inciting HA filler. With regards to the two vaccine related cases; in the mRNA-1273 case, a low dose angiotensin converting enzyme inhibitor (ACE-I) was utilized for treatment, to reduce pro-inflammatory Angiotensin II. Whereas, in the BNT162b2 case the filler reaction was suppressed with oral corticosteroids. Regarding final disposition of the cases; the vaccine-related cases returned to baseline appearance within 3 days, whereas the native COVID-19 case continued to have migratory, evanescent, periorbital edema for weeks which ultimately subsided.


Subject(s)
/adverse effects , COVID-19/virology , Dermal Fillers/adverse effects , Hyaluronic Acid/adverse effects , Inflammation Mediators/immunology , Inflammation/etiology , SARS-CoV-2/pathogenicity , Spike Glycoprotein, Coronavirus/immunology , /administration & dosage , Adult , Anti-Inflammatory Agents/therapeutic use , /immunology , COVID-19/immunology , COVID-19/prevention & control , Diagnosis, Differential , Female , Host-Pathogen Interactions , Humans , Hyaluronic Acid/immunology , Inflammation/drug therapy , Inflammation/immunology , Inflammation/virology , Inflammation Mediators/antagonists & inhibitors , Middle Aged , Risk Assessment , Risk Factors , SARS-CoV-2/immunology , Treatment Outcome , Vaccination/adverse effects
20.
J Diabetes Res ; 2021: 9526701, 2021.
Article in English | MEDLINE | ID: covidwho-1066964

ABSTRACT

The induction of inflammation and cytokine storm was proposed to play a critical role in COVID-19. This study is aimed at investigating the relationship between glucose metabolism and the inflammatory state of inpatients with COVID-19. 71 inpatients with COVID-19 were classified into nondiabetes mellitus (NDM) group, impaired fasting glucose (IFG) group, and diabetes mellitus (DM) group. The average hospitalization days were significantly shorter in DM patients when compared with patients in the IFG group and NDM group. CD4+ T cell percentage was higher while CD8+ T cells percentage was lower in the DM group than those in the NDM group. The serum levels of IL-6, IL-2, IL-10, and INF-γ in the DM group were upregulated when compared with those in the NDM group. The serum levels of TNF-α, IL-4, IL-2, IL-10, and INF-γ were significantly higher in the DM group than those in the IFG group. A significant difference was observed in CD4+ T cell, CD4+/CD8+ ratio percentage, IL-6, and IL-10 between the NDM group and DM group with adjusted BMI. In conclusion, COVID-19 patients with elevated glucose levels have promoted cytokine profiles and immune response.


Subject(s)
CD4-Positive T-Lymphocytes/immunology , CD8-Positive T-Lymphocytes/immunology , COVID-19/immunology , Cytokines/immunology , Diabetes Mellitus, Type 2/immunology , Inflammation Mediators/immunology , SARS-CoV-2/immunology , Adult , Aged , Biomarkers/blood , Blood Glucose/metabolism , CD4-Positive T-Lymphocytes/metabolism , CD4-Positive T-Lymphocytes/virology , CD8-Positive T-Lymphocytes/metabolism , CD8-Positive T-Lymphocytes/virology , COVID-19/blood , COVID-19/epidemiology , COVID-19/virology , Cytokines/blood , Diabetes Mellitus, Type 2/blood , Diabetes Mellitus, Type 2/epidemiology , Female , Host-Pathogen Interactions , Humans , Inflammation Mediators/blood , Length of Stay , Male , Middle Aged , Prognosis , Time Factors
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