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1.
Front Immunol ; 13:1039427, 2022.
Article in English | PubMed | ID: covidwho-2198887

ABSTRACT

In the past two years, the world has faced the pandemic caused by the severe acute respiratory syndrome 2 coronavirus (SARS-CoV-2), which by August of 2022 has infected around 619 million people and caused the death of 6.55 million individuals globally. Although SARS-CoV-2 mainly affects the respiratory tract level, there are several reports, indicating that other organs such as the heart, kidney, pancreas, and brain can also be damaged. A characteristic observed in blood serum samples of patients suffering COVID-19 disease in moderate and severe stages, is a significant increase in proinflammatory cytokines such as interferon-α (IFN-α), interleukin-1β (IL-1β), interleukin-2 (IL-2), interleukin-6 (IL-6) and interleukin-18 (IL-18), as well as the presence of autoantibodies against interferon-α (IFN-α), interferon-λ (IFN-λ), C-C motif chemokine ligand 26 (CCL26), CXC motif chemokine ligand 12 (CXCL12), family with sequence similarity 19 (chemokine (C-C motif)-like) member A4 (FAM19A4), and C-C motif chemokine ligand 1 (CCL1). Interestingly, it has been described that the chronic cytokinemia is related to alterations of blood-brain barrier (BBB) permeability and induction of neurotoxicity. Furthermore, the generation of autoantibodies affects processes such as neurogenesis, neuronal repair, chemotaxis and the optimal microglia function. These observations support the notion that COVID-19 patients who survived the disease present neurological sequelae and neuropsychiatric disorders. The goal of this review is to explore the relationship between inflammatory and humoral immune markers and the major neurological damage manifested in post-COVID-19 patients.

2.
Indian J Clin Biochem ; : 1-8, 2023.
Article in English | Web of Science | ID: covidwho-2175133

ABSTRACT

Immune dysregulation is a key feature of the coronavirus disease-2019 (COVID-19). However, disparities in responses across ethnic groups are underappreciated. This study aimed to determine the relationship between chemokines and cytokines and the severity of COVID-19. Multiplex magnetic bead-based Luminex-100 was used to assess chemokine and cytokine levels in COVID-19 patients at admission (day-1) and after 4 days. The mean age of the patients recruited was 54.3 years, with 19 (63.3%) males. COVID-19 patients had significantly lower lymphocyte, monocyte, hemoglobin and eosinophil levels than controls (p < 0.05). COVID-19 patients showed significantly higher neutrophil levels than controls (p < 0.05). The baseline levels of IL-2, IL-6, IL-8, IL-10, and IFN-alpha/gamma significantly increased in COVID-19 patients (p < 0.05). Chemokine levels (IP-10, MCP-1, MIG, and CCL-5) were significantly in COVID-19 patients. IL-8, IP-10, and MIG levels were significantly higher in the patients with severe COVID-19 (p < 0.05). Individuals with mild COVID-19 showed significantly higher levels of INF-alpha, IL-2, IL-6, and IL-8, whereas IL-10 levels were significantly lower (p < 0.05). TNF-levels decreased significantly in individuals with severe COVID-19, whereas IL-6, IL-8, and MIG levels increased (p < 0.05). After 4 days, INFalpha-, IL-2, IL-6, IL-8, IP-10, and MIG levels were significantly higher in patients with mild disease, whereas IL-6, MIG, and TNF-alphalevels were significantly higher in patients with severe disease (p < 0.05). Thus, we conclude that COVID-19 is characterized by INF-alpha/gamma, IL-6, IL-10, IP-10, MCP-1, MIG, and CCL5 dysregulation. IL-8, MIG, and IP-10 levels distinguish between moderate and severe COVID-19. Changes in INF-alpha, IL-2, IL-6, IL-8, IP-10, and MIG levels can be used to monitor disease progression. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12291-022-01108-x.

3.
International Journal of Molecular Sciences ; 23(24):16071, 2022.
Article in English | ProQuest Central | ID: covidwho-2200325

ABSTRACT

Fusion among different cell populations represents a rare process that is mediated by both intrinsic and extracellular events. Cellular hybrid formation is relayed by orchestrating tightly regulated signaling pathways that can involve both normal and neoplastic cells. Certain important cell merger processes are often required during distinct organismal and tissue development, including placenta and skeletal muscle. In a neoplastic environment, however, cancer cell fusion can generate new cancer hybrid cells. Following survival during a subsequent post-hybrid selection process (PHSP), the new cancer hybrid cells express different tumorigenic properties. These can include elevated proliferative capacity, increased metastatic potential, resistance to certain therapeutic compounds, and formation of cancer stem-like cells, all of which characterize significantly enhanced tumor plasticity. However, many parts within this multi-step cascade are still poorly understood. Aside from intrinsic factors, cell fusion is particularly affected by extracellular conditions, including an inflammatory microenvironment, viruses, pH and ionic stress, hypoxia, and exosome signaling. Accordingly, the present review article will primarily highlight the influence of extracellular events that contribute to cell fusion in normal and tumorigenic tissues.

4.
International Journal of Molecular Sciences ; 23(24):15823, 2022.
Article in English | ProQuest Central | ID: covidwho-2200320

ABSTRACT

Several studies have indicated that a neutrophil extracellular trap (NET) formation, apart from its role in host defense, can contribute to or drive pathogenesis in a wide range of inflammatory and thrombotic disorders. Therefore, NETs may serve as a therapeutic target or/and a diagnostic tool. Here, we compare the most commonly used techniques for the assessment of NET formation. Furthermore, we review recent data from the literature on the application of basic laboratory tools for detecting NET release and discuss the challenges and the advantages of these strategies in NET evaluation. Taken together, we provide some important insights into the qualitative and quantitative molecular analysis of NETs in translational medicine today.

5.
European Journal of Biological Research ; 12(4):307-319, 2022.
Article in English | ProQuest Central | ID: covidwho-2202667

ABSTRACT

Through the emeigence of new viral infectious diseases, epidemics and pandemics have brought great impacts on public health in recent decades. In this review, we sought to understand the association between the neurological outcomes of two relevant infectious diseases, Zika and COVID-19. Zika can trigger neurological and ophthalmic damage in children born from infected mothers, as well as, Guillain-Barré syndrome, encephalitis, and myelitis in adults. On the other hand, the SARS-CoV-2 virus has great potential to trigger an inflammatory process in the optic nerve, with optic neuritis as the most reported pathology. Although Zika and SARS-CoV-2 infections are associated with different clinical manifestations, both may trigger similar pathogenic processes, through the induction of pro-inflammatory chemokines and cytokines release, triggering neurological and ophthalmological damage in infected patients. Elements in common have been found in both infections, such as antibodies against myelin oligodendrocyte glycoprotein, and the production of CXCL10, a chemokine responsible for the activation of several cellular types (T cells, eosinophils, monocytes and NK cells) in which are responsible to the induction of a cytokine cascade in the body. Based on these last findings, we suggest that both infections have similar activation characteristics as well as common pathogenic mechanisms associated with central nervous system involvement.

6.
Viruses ; 14(11)2022 Nov 03.
Article in English | MEDLINE | ID: covidwho-2200863

ABSTRACT

Chemokines constitute a group of small, secreted proteins that regulate leukocyte migration and contribute to their activation. Chemokines are crucial inflammatory mediators that play a key role in managing viral infections, during which the profile of chemokine expression helps shape the immune response and regulate viral clearance, improving clinical outcome. In particular, the chemokine ligand CXCL10 and its receptor CXCR3 were explored in a plethora of RNA and DNA viral infections. In this review, we highlight the expression profile and role of the CXCL10/CXCR3 axis in the host defense against a variety of RNA and DNA viral infections. We also discuss the interactions among viruses and host cells that trigger CXCL10 expression, as well as the signaling cascades induced in CXCR3 positive cells.


Subject(s)
Chemokine CXCL10 , Virus Diseases , Humans , Chemokine CXCL10/genetics , RNA , Virus Diseases/genetics , DNA
7.
Front Immunol ; 13: 931388, 2022.
Article in English | MEDLINE | ID: covidwho-2141951

ABSTRACT

Intracranial inoculation of the neuroadapted JHM strain of mouse hepatitis virus (JHMV) into susceptible strains of mice results in acute encephalomyelitis followed by a cimmune-mediated demyelination similar to the human demyelinating disease multiple sclerosis (MS). JHMV infection of transgenic mice in which expression of the neutrophil chemoattractant chemokine CXCL1 is under the control of a tetracycline-inducible promoter active within GFAP-positive cells results in sustained neutrophil infiltration in the central nervous system (CNS) that correlates with an increase in spinal cord demyelination. We used single cell RNA sequencing (scRNAseq) and flow cytometry to characterize molecular and cellular changes within the CNS associated with increased demyelination in transgenic mice compared to control animals. These approaches revealed the presence of activated neutrophils as determined by expression of mRNA transcripts associated with neutrophil effector functions, including CD63, MMP9, S100a8, S100a9, and ASPRV1, as well as altered neutrophil morphology and protein expression. Collectively, these findings reveal insight into changes in the profile of neutrophils associated with increased white matter damage in mice persistently infected with a neurotropic coronavirus.


Subject(s)
Demyelinating Diseases , Multiple Sclerosis , Murine hepatitis virus , White Matter , Animals , Central Nervous System , Chemokine CXCL1/metabolism , Humans , Matrix Metalloproteinase 9/metabolism , Mice , Mice, Transgenic , Multiple Sclerosis/metabolism , Neutrophils/metabolism , RNA, Messenger , Tetracyclines , White Matter/metabolism
8.
Vet Microbiol ; 275: 109599, 2022 Dec.
Article in English | MEDLINE | ID: covidwho-2132637

ABSTRACT

Porcine epidemic diarrhea virus (PEDV) is a re-emerging pathogen that causes severe economic loss in the pig industry. The host's innate immune system is the first line of defense on virus invasion of the small intestinal epithelial cells. Chemokines, as a part of the innate immune system, play an important role in host immunity against infection, however, and their expression and chemotactic effect on key immune cells in PEDV infection remains unclear. In this study, cDNA microarray was firstly performed to analyzed ileum tissue of piglets on the third day after PEDV infection. The differentially expressed genes mainly involved in multiple biological processes, chemokine signaling pathway and cytokine receptor interaction signaling pathway had the highest enrichment according to GO and KEGG enrichment analysis. The expression levels of chemokines MCP-1, MIP-1ß, IL-8, CXCL9, CXCL10 and CXCL13 in ileum of PEDV- infected piglets were significantly higher than those in the control group. The expression of chemokines in vivo experiment was further verified by RT-qPCR and ELISA using PEDV-infected IPEC-J2 cells. The results showed that the PEDV-infected IPEC-J2 cells had significantly induced protein expression of MCP-1, MIP-1ß, IL-8, CXCL9, CXCL-10 and CXCL13. These results indicated that the changes of chemokines expressed in the ileum of piglets (in vivo) were consistent with those in IPEC-J2 cells (in vitro) after PEDV infection. Finally, the role of chemokines in immune cell migration during PEDV infection was illustrated by siRNA-mediated knock down method and the co-culture model of IPEC-J2 cells with peripheral blood leukocyte cells (PBLCs). The FACS analysis showed that MCP-1 induced by PEDV infection played a chemotactic effect on CD14+ cells, CXCL9 on CD3+CD4-CD8-γδ T, CD3+CD4-CD8+ Tc, CD3+CD4+CD8- Th and CD3+CD4+CD8+ Tm subsets, and CXCL13 on CD19+ B cells. Collectively, our findings first indicate that PEDV-induced chemokines MCP-1, CXCL-9 and CXCL-13 attracted CD14+ cells, T cells and B cells, respectively. These results provide a theoretical basis for studying the mechanism of anti-PEDV infection in piglets.


Subject(s)
Coronavirus Infections , Porcine epidemic diarrhea virus , Swine Diseases , Animals , Swine , Monocytes , Chemokine CCL4/pharmacology , Interleukin-8/genetics , Coronavirus Infections/veterinary , Cell Line
9.
Transl Med Commun ; 7(1): 3, 2022.
Article in English | MEDLINE | ID: covidwho-2098471

ABSTRACT

Background: Dysregulation of antiviral immunity has been implicated in the progression of acute respiratory syndrome coronavirus 2 infection into severe cases of coronavirus disease of 2019 (COVID-19). Imbalances in the inflammatory response drive the overabundant production of pro-inflammatory cytokines and chemokines. The low molecular weight fraction of 5% human serum albumin commercial preparation (AMP5A) is a novel biologic drug currently under clinical investigation for the treatment of osteoarthritis and the hyperinflammatory response associated with COVID-19. This study aims to elucidate AMP5A effects following the activation of immune cells with agonists of Toll-like receptor (TLR) 7 and/or 8, which detect ssRNA viral sequences. Methods: CXCL10 ELISAs were used to evaluate the dynamics of myeloid cells activated with CL075 and CL307, agonists of TLR7/8 and TLR7, respectively. In addition, enrichment analysis of gene sets generated by ELISA arrays was utilized to gain insight into the biologic processes underlying the identified differentially expressed cytokine profiles. Finally, relative potency (REP) was employed to confirm the involvement of mechanisms of action paramount to AMP5A activity. Results: AMP5A inhibits the release of CXCL10 from both CL075- and CL307-activated PMA-differentiated THP-1 and peripheral blood mononuclear cells. Furthermore, AMP5A suppresses a distinct set of pro-inflammatory cytokines (including IL-1ß, IL-6, IL-12, and CXCL10) associated with COVID-19 and pro-inflammatory NF-κB activation. REP experiments using antagonists specific for the immunomodulatory transcription factors, peroxisome proliferator-activated receptor γ, and aryl hydrocarbon receptor, also indicate that these pathways are involved in the ability of AMP5A to inhibit CXCL10 release. Conclusion: Due to the biphasic course of COVID-19, therapeutic approaches that augment antiviral immunity may be more beneficial early in infection, whereas later interventions should focus on inflammation suppression. In this study, we show that AMP5A inhibits TLR 7/8 signaling in myeloid cells, resulting in a decrease in inflammatory mediators associated with hyperinflammation and autoimmunity. Furthermore, data demonstrating that AMP5A activates immunomodulatory transcription factors found to be protective in lung disease is provided. These findings suggest that the modes and mechanisms of action of AMP5A are well suited to treat conditions involving dysregulated TLR 7/8 activation.

10.
Int J Mol Sci ; 23(21)2022 Oct 22.
Article in English | MEDLINE | ID: covidwho-2081827

ABSTRACT

Systemic juvenile idiopathic arthritis (sJIA) and its complication, macrophage activation syndrome (sJIA-MAS), are rare but sometimes very serious or even critical diseases of childhood that can occasionally be characterized by nonspecific clinical signs and symptoms at onset-such as non-remitting high fever, headache, rash, or arthralgia-and are biologically accompanied by an increase in acute-phase reactants. For a correct positive diagnosis, it is necessary to rule out bacterial or viral infections, neoplasia, and other immune-mediated inflammatory diseases. Delays in diagnosis will result in late initiation of targeted therapy. A set of biomarkers is useful to distinguish sJIA or sJIA-MAS from similar clinical entities, especially when arthritis is absent. Biomarkers should be accessible to many patients, with convenient production and acquisition prices for pediatric medical laboratories, as well as being easy to determine, having high sensitivity and specificity, and correlating with pathophysiological disease pathways. The aim of this review was to identify the newest and most powerful biomarkers and their synergistic interaction for easy and accurate recognition of sJIA and sJIA-MAS, so as to immediately guide clinicians in correct diagnosis and in predicting disease outcomes, the response to treatment, and the risk of relapses. Biomarkers constitute an exciting field of research, especially due to the heterogeneous nature of cytokine storm syndromes (CSSs) in the COVID era. They must be selected with utmost care-a fact supported by the increasingly improved genetic and pathophysiological comprehension of sJIA, but also of CSS-so that new classification systems may soon be developed to define homogeneous groups of patients, although each with a distinct disease.


Subject(s)
Arthritis, Juvenile , COVID-19 , Macrophage Activation Syndrome , Humans , Child , Macrophage Activation Syndrome/diagnosis , Macrophage Activation Syndrome/drug therapy , Macrophage Activation Syndrome/etiology , Arthritis, Juvenile/diagnosis , Arthritis, Juvenile/drug therapy , COVID-19/diagnosis , Biomarkers
11.
Front Immunol ; 13: 1008438, 2022.
Article in English | MEDLINE | ID: covidwho-2080155

ABSTRACT

Objectives: To determine the profile of cytokines in patients with severe COVID-19 who were enrolled in a trial of COVID-19 convalescent plasma (CCP). Methods: Patients were randomized to receive standard treatment and 3 CCP units or standard treatment alone (CAPSID trial, ClinicalTrials.gov NCT04433910). The primary outcome was a dichotomous composite outcome (survival and no longer severe COVID-19 on day 21). Time to clinical improvement was a key secondary endpoint. The concentrations of 27 cytokines were measured (baseline, day 7). We analyzed the change and the correlation between serum cytokine levels over time in different subgroups and the prediction of outcome in receiver operating characteristics (ROC) analyses and in multivariate models. Results: The majority of cytokines showed significant changes from baseline to day 7. Some were strongly correlated amongst each other (at baseline the cluster IL-1ß, IL-2, IL-6, IL-8, G-CSF, MIP-1α, the cluster PDGF-BB, RANTES or the cluster IL-4, IL-17, Eotaxin, bFGF, TNF-α). The correlation matrix substantially changed from baseline to day 7. The heatmaps of the absolute values of the correlation matrix indicated an association of CCP treatment and clinical outcome with the cytokine pattern. Low levels of IP-10, IFN-γ, MCP-1 and IL-1ß on day 0 were predictive of treatment success in a ROC analysis. In multivariate models, low levels of IL-1ß, IFN-γ and MCP-1 on day 0 were significantly associated with both treatment success and shorter time to clinical improvement. Low levels of IP-10, IL-1RA, IL-6, MCP-1 and IFN-γ on day 7 and high levels of IL-9, PDGF and RANTES on day 7 were predictive of treatment success in ROC analyses. Low levels of IP-10, MCP-1 and high levels of RANTES, on day 7 were associated with both treatment success and shorter time to clinical improvement in multivariate models. Conclusion: This analysis demonstrates a considerable dynamic of cytokines over time, which is influenced by both treatment and clinical course of COVID-19. Levels of IL-1ß and MCP-1 at baseline and MCP-1, IP-10 and RANTES on day 7 were associated with a favorable outcome across several endpoints. These cytokines should be included in future trials for further evaluation as predictive factors.


Subject(s)
COVID-19 , Cytokines , Humans , Interleukin 1 Receptor Antagonist Protein , Interleukin-17 , Chemokine CCL3 , Tumor Necrosis Factor-alpha , Interleukin-6 , Interleukin-4 , Capsid , COVID-19/therapy , Becaplermin , Chemokine CXCL10 , Interleukin-2 , Interleukin-8 , Interleukin-9 , Granulocyte Colony-Stimulating Factor
13.
Biomedicines ; 10(9)2022 Sep 19.
Article in English | MEDLINE | ID: covidwho-2032844

ABSTRACT

The purpose of this study was to examine the effect of the JAK-STAT inhibitor baricitinib on the inflammatory response of human monocyte-derived macrophages (MDM) and endothelial cells upon exposure to the spike S1 protein from SARS-CoV-2. The effect of the drug has been evaluated on the release of cytokines and chemokines from spike-treated MDM, as well as on the activation of endothelial cells (HUVECs) after exposure to conditioned medium collected from spike-activated MDM. Results obtained indicate that, in MDM, baricitinib prevents the S1-dependent phosphorylation of STAT1 and STAT3, along with the induction of IP-10- and MCP-1 secretion; the release of IL-6 and TNFα is also reduced, while all other mediators tested (IL-1ß, IL-8, RANTES, MIP-1α and MIP-1ß) are not modified. Baricitinib is, instead, poorly effective on endothelial activation when HUVECs are exposed to supernatants from S1-activated macrophages; the induction of VCAM-1, indeed, is not affected by the drug, while that of ICAM-1 is only poorly inhibited. The drug, however, also exerts protective effects on the endothelium by limiting the expression of pro-inflammatory mediators, specifically IL-6, RANTES and IP-10. No effect of baricitinib has been observed on IL-8 synthesis and, consistently, on neutrophils chemiotaxis. Our in vitro findings reveal that the efficacy of baricitinib is limited, with effects mainly focused on the inhibition of the IL-6-mediated inflammatory loop.

14.
Gülhane Tip Dergisi ; 64(3):208-216, 2022.
Article in English | ProQuest Central | ID: covidwho-2024906

ABSTRACT

We assessed the blood levels of the most important factors such as cytokines/chemokines in Coronavirus disease-2019 (COVID-19). PubMed/Medline and Scopus as two important databases were searched up to March 26, 2020. To analyze the data, we used Review Manager 5.3 software. Out of forty-two records retrieved from two databases, 10 studies were involved in the analysis. Thirty-three cytokines/chemokines were checked. The levels of 27 cytokines/chemokines in COVID-19 patients were higher than the healthy controls, and among 20 cytokines/chemokines;the levels of 10 cytokines/chemokines in severe COVID-19 patients were higher than non-severe COVID-19 patients. Also, out of three cytokines, one had a higher level in the intensive care unit (ICU) patients compared to the non-ICU patients. The findings showed the cytokine storm syndrome in COVID-19 patients, especially in patients with severe disease.

15.
Int J Mol Sci ; 23(18)2022 Sep 07.
Article in English | MEDLINE | ID: covidwho-2010121

ABSTRACT

SARS-CoV-2 is a new coronavirus characterized by a high infection and transmission capacity. A significant number of patients develop inadequate immune responses that produce massive releases of cytokines that compromise their survival. Soluble factors are clinically and pathologically relevant in COVID-19 survival but remain only partially characterized. The objective of this work was to simultaneously study 62 circulating soluble factors, including innate and adaptive cytokines and their soluble receptors, chemokines and growth and wound-healing/repair factors, in severe COVID-19 patients who survived compared to those with fatal outcomes. Serum samples were obtained from 286 COVID-19 patients and 40 healthy controls. The 62 circulating soluble factors were quantified using a Luminex Milliplex assay. Results. The patients who survived had decreased levels of the following 30 soluble factors of the 62 studied compared to those with fatal outcomes, therefore, these decreases were observed for cytokines and receptors predominantly produced by the innate immune system-IL-1α, IL-1α, IL-18, IL-15, IL-12p40, IL-6, IL-27, IL-1Ra, IL-1RI, IL-1RII, TNFα, TGFα, IL-10, sRAGE, sTNF-RI and sTNF-RII-for the chemokines IL-8, IP-10, MCP-1, MCP-3, MIG and fractalkine; for the growth factors M-CSF and the soluble receptor sIL2Ra; for the cytokines involved in the adaptive immune system IFNγ, IL-17 and sIL-4R; and for the wound-repair factor FGF2. On the other hand, the patients who survived had elevated levels of the soluble factors TNFß, sCD40L, MDC, RANTES, G-CSF, GM-CSF, EGF, PDGFAA and PDGFABBB compared to those who died. Conclusions. Increases in the circulating levels of the sCD40L cytokine; MDC and RANTES chemokines; the G-CSF and GM-CSF growth factors, EGF, PDGFAA and PDGFABBB; and tissue-repair factors are strongly associated with survival. By contrast, large increases in IL-15, IL-6, IL-18, IL-27 and IL-10; the sIL-1RI, sIL1RII and sTNF-RII receptors; the MCP3, IL-8, MIG and IP-10 chemokines; the M-CSF and sIL-2Ra growth factors; and the wound-healing factor FGF2 favor fatal outcomes of the disease.


Subject(s)
COVID-19 , Interleukin-27 , Chemokine CCL5 , Chemokine CX3CL1 , Chemokine CXCL10 , Cytokines , Epidermal Growth Factor , Fibroblast Growth Factor 2 , Granulocyte Colony-Stimulating Factor , Granulocyte-Macrophage Colony-Stimulating Factor , Humans , Interleukin 1 Receptor Antagonist Protein , Interleukin-10 , Interleukin-12 Subunit p40 , Interleukin-15 , Interleukin-17 , Interleukin-18 , Interleukin-6 , Interleukin-8 , Macrophage Colony-Stimulating Factor , SARS-CoV-2 , Transforming Growth Factor alpha , Tumor Necrosis Factor-alpha
16.
Zhongguo Bingyuan Shengwuxue Zazhi / Journal of Pathogen Biology ; 15(4):458-461, 2020.
Article in Chinese | GIM | ID: covidwho-1994548

ABSTRACT

Objectives: To investigate pathogenic bacteria, their drug resistance, and changes in levels of cytokines in patients with a puerperal infection after a Cesarean section.

17.
Vaccines (Basel) ; 10(8)2022 Aug 11.
Article in English | MEDLINE | ID: covidwho-1988049

ABSTRACT

COVID-19 is one of the progressive viral pandemics that originated from East Asia. COVID-19 or SARS-CoV-2 has been shown to be associated with a chain of physio-pathological mechanisms that are basically immunological in nature. In addition, chemokines have been proposed as a subgroup of chemotactic cytokines with different activities ranging from leukocyte recruitment to injury sites, irritation, and inflammation to angiostasis and angiogenesis. Therefore, researchers have categorized the chemotactic elements into four classes, including CX3C, CXC, CC, and C, based on the location of the cysteine motifs in their structures. Considering the severe cases of COVID-19, the hyperproduction of particular chemokines occurring in lung tissue as well as pro-inflammatory cytokines significantly worsen the disease prognosis. According to the studies conducted in the field documenting the changing expression of CXC and CC chemokines in COVID-19 cases, the CC and CXC chemokines contribute to this pandemic, and their impact could reflect the development of reasonable strategies for COVID-19 management. The CC and the CXC families of chemokines are important in host immunity to viral infections and along with other biomarkers can serve as the surrogates of vaccine-induced innate and adaptive protective responses, facilitating the improvement of vaccine efficacy. Furthermore, the immunogenicity elicited by the chemokine response to adenovirus vector vaccines may constitute the basis of vaccine-induced immune thrombotic thrombocytopaenia.

18.
Int J Mol Sci ; 23(16)2022 Aug 13.
Article in English | MEDLINE | ID: covidwho-1987830

ABSTRACT

BACKGROUND: Infection caused by SARS-CoV-2 mostly affects the upper and lower respiratory tracts and causes symptoms ranging from the common cold to pneumonia with acute respiratory distress syndrome. Chemokines are deeply involved in the chemoattraction, proliferation, and activation of immune cells within inflammation. It is crucial to consider that mutations within the virion can potentially affect the clinical course of SARS-CoV-2 infection because disease severity and manifestation vary depending on the genetic variant. Our objective was to measure and assess the different concentrations of chemokines involved in COVID-19 caused by different variants of the virus. METHODS: We used the blood plasma of patients infected with different variants of SARS-CoV-2, i.e., the ancestral Wuhan strain and the Alpha, Delta, and Omicron variants. We measured the concentrations of 11 chemokines in the samples: CCL2/MCP-1, CCL3/MIP-1α, CCL4/MIP-1ß, CCL7/MCP-3, CCL11/Eotaxin, CCL22/MDC, CXCL1/GROα, CXCL8/IL-8, CXCL9/MIG, CXCL10/IP-10, and CX3CL1/Fractalkine. RESULTS: We noted a statistically significant elevation in the concentrations of CCL2/MCP-1, CXCL8/IL-8, and CXCL1/IP-10 independently of the variant, and a drop in the CCL22/MDC concentrations. CONCLUSIONS: The chemokine concentrations varied significantly depending on the viral variant, leading us to infer that mutations in viral proteins play a role in the cellular and molecular mechanisms of immune responses.


Subject(s)
COVID-19 , SARS-CoV-2 , COVID-19/immunology , Chemokine CXCL10 , Chemokines/blood , Humans , Interleukin-8 , Plasma
19.
Front Immunol ; 13: 887503, 2022.
Article in English | MEDLINE | ID: covidwho-1987492

ABSTRACT

Natural killer (NK) cells are an important component of the innate immune system, and have a key role in host defense against infection and in tumor surveillance. Tumors and viruses employ remarkably similar strategies to avoid recognition and killing by NK cells and so much can be learnt by comparing NK cells in these disparate diseases. The lung is a unique tissue environment and immune cells in this organ, including NK cells, exist in a hypofunctional state to prevent activation against innocuous stimuli. Upon infection, rapid NK cell infiltration into the lung occurs, the amplitude of which is determined by the extent of inflammation and damage. Activated NK cells kill infected cells and produce pro-inflammatory cytokines and chemokines to recruit cells of the adaptive immune system. More recent evidence has shown that NK cells also play an additional role in resolution of inflammation. In lung cancer however, NK cell recruitment is impaired and those that are present have reduced functionality. The majority of lung NK cells are circulatory, however recently a small population of tissue-resident lung NK cells has been described. The specific role of this subset is yet to be determined, but they show similarity to resident memory T cell subsets. Whether resident or recruited, NK cells are important in the control of pulmonary infections, but equally, can drive excessive inflammation if not regulated. In this review we discuss how NK cells are recruited, controlled and retained in the specific environment of the lung in health and disease. Understanding these mechanisms in the context of infection may provide opportunities to promote NK cell recruitment and function in the lung tumor setting.


Subject(s)
Killer Cells, Natural , Lung Neoplasms , Cytokines , Humans , Inflammation , Lung
20.
J Infect Dis ; 226(7): 1215-1223, 2022 09 28.
Article in English | MEDLINE | ID: covidwho-1985078

ABSTRACT

BACKGROUND: Multisystem inflammatory syndrome in children (MIS-C) presents with inflammation and pathology of multiple organs in the pediatric population in the weeks following severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. METHODS: We characterized the SARS-CoV-2 antigen-specific cytokine and chemokine responses in children with MIS-C, coronavirus disease 2019 (COVID-19), and other infectious diseases. RESULTS: MIS-C is characterized by elevated levels of type 1 (interferon-γ, interleukin [IL] 2), type 2 (IL-4, IL-13), type 17 (IL-17), and other proinflammatory cytokines (IL-1α, IL-6, IL-12p70, IL-18, and granulocyte-macrophage colony-stimulating factor) in comparison to COVID-19 and other infectious diseases following stimulation with SARS-CoV-2-specific antigens. Similarly, upon SARS-CoV-2 antigen stimulation, CCL2, CCL3, and CXCL10 chemokines were significantly elevated in children with MIS-C in comparison to the other 2 groups. Principal component analysis based on these cytokines and chemokines could clearly distinguish MIS-C from both COVID-19 and other infections. In addition, these responses were significantly diminished and normalized 6-9 months after recovery. CONCLUSIONS: Our data suggest that MIS-C is characterized by an enhanced production of cytokines and chemokines that may be associated with disease pathogenesis.


Subject(s)
COVID-19 , Communicable Diseases , Antigens, Viral , COVID-19/complications , Chemokines , Child , Cytokines , Granulocyte-Macrophage Colony-Stimulating Factor , Humans , Immunity , Interferon-gamma , Interleukin-13 , Interleukin-17 , Interleukin-18 , Interleukin-4 , Interleukin-6 , SARS-CoV-2 , Systemic Inflammatory Response Syndrome
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