scholarly journals Cytokine Storm Syndrome in SARS-CoV-2 Infections: A Functional Role of Mast Cells

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1761
Author(s):  
Bahareh Hafezi ◽  
Lily Chan ◽  
Jason P. Knapp ◽  
Negar Karimi ◽  
Kimia Alizadeh ◽  
...  
Keyword(s):  
Mast Cell ◽  
Immune System ◽  
Mast Cells ◽  
Severe Acute Respiratory Syndrome ◽  
Immune Responses ◽  
Functional Role ◽  
Cytokine Storm ◽  
Proper Treatment ◽  
Present Evidence

Cytokine storm syndrome is a cascade of escalated immune responses disposing the immune system to exhaustion, which might ultimately result in organ failure and fatal respiratory distress. Infection with severe acute respiratory syndrome-coronavirus-2 can result in uncontrolled production of cytokines and eventually the development of cytokine storm syndrome. Mast cells may react to viruses in collaboration with other cells and lung autopsy findings from patients that died from the coronavirus disease that emerged in 2019 (COVID-19) showed accumulation of mast cells in the lungs that was thought to be the cause of pulmonary edema, inflammation, and thrombosis. In this review, we present evidence that a cytokine response by mast cells may initiate inappropriate antiviral immune responses and cause the development of cytokine storm syndrome. We also explore the potential of mast cell activators as adjuvants for COVID-19 vaccines and discuss the medications that target the functions of mast cells and could be of value in the treatment of COVID-19. Recognition of the cytokine storm is crucial for proper treatment of patients and preventing the release of mast cell mediators, as impeding the impacts imposed by these mediators could reduce the severity of COVID-19.

scholarly journals Platelet Function in Viral Immunity and SARS-CoV-2 Infection

2021 ◽  
Author(s):  
Afaf Allaoui ◽  
Akif A. Khawaja ◽  
Oussama Badad ◽  
Mariam Naciri ◽  
Marie Lordkipanidzé ◽  
...  
Keyword(s):  
Severe Acute Respiratory Syndrome ◽  
Infectious Diseases ◽  
Immune Responses ◽  
Cytokine Storm ◽  
Blood Components ◽  
Viral Immunity ◽  
Cytokines And Chemokines ◽  
Activated Platelets ◽  
Viral Receptors

AbstractPlatelets, as nonnucleated blood components, are classically recognized for their pivotal role in hemostasis. In recent years, however, accumulating evidence points to a nonhemostatic role for platelets, as active participants in the inflammatory and immune responses to microbial organisms in infectious diseases. This stems from the ability of activated platelets to secrete a plethora of immunomodulatory cytokines and chemokines, as well as directly interplaying with viral receptors. While much attention has been given to the role of the cytokine storm in the severity of the coronavirus disease 2019 (COVID-19), less is known about the contribution of platelets to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Here, we give a brief overview on the platelet contribution to antiviral immunity and response during SARS-CoV-2 infection.

scholarly journals Cytokines mediated hyperinflammation in SARS-CoV2: An Overview

2020 ◽  
Vol 1 (supplement) ◽  
pp. 7
Author(s):  
Liaqat Ali
Keyword(s):  
Middle East ◽  
Severe Acute Respiratory Syndrome ◽  
Immune Responses ◽  
T Lymphocyte ◽  
Lymphoid Tissue ◽  
Inflammatory Responses ◽  
Cytokine Storm ◽  
Host Immune Responses ◽  
Lymphocyte Responses

Hyperinflammation induced by Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV2) is a major cause of disease severity and mortality in infected patients. The immunopathogenesis of SARS-CoV2 infection is similar to the previous Middle East Respiratory Syndrome-related coronavirus (MERS-CoV) and SARS-CoV coronavirus with severe inflammatory responses. Therefore, severity of this viral infection is not only associated with the virus but also due to host immune responses. Hyperinflammatory responses due to cytokine storm are a centerpiece of SARS-CoV2 pathogenesis with overwhelming consequences for the host. Virus infected monocyte derived macrophages produce cytokines and this contributes to damage of lymphoid tissue and limits the lymphocyte responses. Blocking the deadly cytokine storm and T lymphocyte stimulation is a vital defense for treating SARS-CoV2. Here, we will describe the role of hyperinflamation and the involvement of cytokines in severe SARS-CoV2 infection.

scholarly journals Mast Cell and Autoimmune Diseases

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Yunzhi Xu ◽  
Guangjie Chen
Keyword(s):  
Rheumatoid Arthritis ◽  
Multiple Sclerosis ◽  
Mast Cell ◽  
Immune System ◽  
Mast Cells ◽  
Autoimmune Diseases ◽  
Innate Immune System ◽  
Innate Immune ◽  
Current Stage

Mast cells are important in innate immune system. They have been appreciated as potent contributors to allergic reaction. However, increasing evidence implicates the important role of mast cells in autoimmune disease like rheumatoid arthritis and multiple sclerosis. Here we review the current stage of knowledge about mast cells in autoimmune diseases.

Expression, epitope analysis, and functional role of the LFA-2 antigen detectable on neoplastic mast cells

Blood ◽  
2001 ◽  
Vol 98 (13) ◽  
pp. 3784-3792 ◽  
Author(s):  
Gerit-Holger Schernthaner ◽  
John-Hendrik Jordan ◽  
Minoo Ghannadan ◽  
Hermine Agis ◽  
Dorian Bevec ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Messenger Rna ◽  
Functional Role ◽  
Systemic Mastocytosis ◽  
Cell Leukemia ◽  
Natural Ligand ◽  
Mast Cell Leukemia ◽  
And Function

Abstract Recent data suggest that mast cells (MCs) in patients with systemic mastocytosis or mast cell leukemia express a CD2-reactive antigen. To explore the biochemical nature and function of this antigen, primary MCs as well as the MC line HMC-1 derived from a patient with mast cell leukemia were examined. Northern blot experiments revealed expression of CD2 messenger RNA in HMC-1, whereas primary nonneoplastic MCs did not express transcripts for CD2. In cell surface staining experiments, bone marrow (BM) MCs in systemic mastocytosis (n = 12) as well as HMC-1 cells (30%-80%) were found to express the T11-1 and T11-2 (but not T11-3) epitopes of CD2. By contrast, BM MCs in myelodysplastic syndromes and nonhematologic disorders (bronchiogenic carcinoma, foreskin phimosis, uterine myeomata ) were consistently CD2−. All MC species analyzed including HMC-1 were found to express LFA-3 (CD58), the natural ligand of CD2. To study the functional role of CD2 on neoplastic MCs, CD2+ and CD2− HMC-1 cells were separated by cell sorting. CD2+ HMC-1 cells were found to form spontaneous aggregates and rosettes with sheep erythrocytes in excess over CD2−cells, and a T11-1 antibody inhibited both the aggregation and rosette formation. Moreover, exposure of CD2+ HMC-1 cells to T11-1 or T11-2 antibody was followed by expression of T11-3. In addition, stimulation of neoplastic MCs through T11-3 and a second CD2 epitope resulted in histamine release. These data show that neoplastic MCs express functionally active CD2. It is hypothesized that expression of CD2 is associated with pathologic accumulation and function of MCs in systemic mastocytosis.

scholarly journals The mast cell–B cell axis in lung vascular remodeling and pulmonary hypertension

2017 ◽  
Vol 312 (5) ◽  
pp. L710-L721 ◽  
Author(s):  
Siegfried Breitling ◽  
Zhang Hui ◽  
Diana Zabini ◽  
Yijie Hu ◽  
Julia Hoffmann ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Mast Cell ◽  
Immune System ◽  
B Cells ◽  
Mast Cells ◽  
B Cell ◽  
Vascular Remodeling ◽  
Critical Role ◽  
Cell Axis

Over past years, a critical role for the immune system and, in particular, for mast cells in the pathogenesis of pulmonary hypertension (PH) has emerged. However, the way in which mast cells promote PH is still poorly understood. Here, we investigated the mechanisms by which mast cells may contribute to PH, specifically focusing on the interaction between the innate and adaptive immune response and the role of B cells and autoimmunity. Experiments were performed in Sprague-Dawley rats and B cell-deficient JH-KO rats in the monocrotaline, Sugen/hypoxia, and the aortic banding model of PH. Hemodynamics, cell infiltration, IL-6 expression, and vascular remodeling were analyzed. Gene array analyses revealed constituents of immunoglobulins as most prominently regulated mast cell-dependent genes in the lung in experimental PH. IL-6 was shown to link mast cells to B cells, as 1) IL-6 was upregulated and colocalized with mast cells and was reduced by mast-cell stabilizers and 2) IL-6 or mast cell blockade reduced B cells in lungs of monocrotaline-treated rats. A functional role for B cells in PH was demonstrated in that either blocking B cells by an anti-CD20 antibody or B-cell deficiency in JH-KO rats attenuated right ventricular systolic pressure and vascular remodeling in experimental PH. We here identify a mast cell–B cell axis driven by IL-6 as a critical immune pathway in the pathophysiology of PH. Our results provide novel insights into the role of the immune system in PH, which may be therapeutically exploited by targeted immunotherapy.

scholarly journals Thromboses and Hemostasis Disorders Associated with Coronavirus Disease 2019: The Possible Causal Role of Cross-Reactivity and Immunological Imprinting

2021 ◽  
Author(s):  
Darja Kanduc
Keyword(s):  
Immune System ◽  
Severe Acute Respiratory Syndrome ◽  
Natural Infection ◽  
Vascular Diseases ◽  
Cross Reactivity ◽  
Active Immunization ◽  
Thromboembolic Complications ◽  
Human Proteins ◽  
Almost All

AbstractBy examining the issue of the thromboses and hemostasis disorders associated with severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) through the lens of cross-reactivity, it was found that 60 pentapeptides are shared by SARS-CoV-2 spike glycoprotein (gp) and human proteins that— when altered, mutated, deficient or, however, improperly functioning— cause vascular diseases, thromboembolic complications, venous thrombosis, thrombocytopenia, coagulopathies, and bleeding, inter alia. The peptide commonality has a relevant immunological potential as almost all of the shared sequences are present in experimentally validated SARS-CoV-2 spike gp-derived epitopes, thus supporting the possibility of cross-reactions between the viral gp and the thromboses-related human proteins. Moreover, many of the shared peptide sequences are also present in pathogens to which individuals have previously been exposed following natural infection or vaccinal routes, and of which the immune system has stored imprint. Such an immunological memory might rapidly trigger anamnestic secondary cross-reactive responses of extreme affinity and avidity, in this way explaining the thromboembolic adverse events that can associate with SARS-CoV-2 infection or active immunization.

Comparative analysis of the role of mast cells in murine asthma models using Kit‐sufficient mast cell‐deficient animals

Allergy ◽  
2021 ◽  
Author(s):  
Lea Pohlmeier ◽  
Sanchaita Sriwal Sonar ◽  
Hans‐Reimer Rodewald ◽  
Manfred Kopf ◽  
Luigi Tortola
Keyword(s):  
Mast Cell ◽  
Comparative Analysis ◽  
Mast Cells

Mast cell heterogeneity

1984 ◽  
Vol 62 (6) ◽  
pp. 734-737 ◽  
Author(s):  
F. Shanahan ◽  
J. A. Denburg ◽  
J. Bienenstock ◽  
A. D. Befus
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Connective Tissue ◽  
Regulatory Peptides ◽  
Cell Heterogeneity ◽  
Cell Secretion ◽  
Biochemical Basis ◽  
Mucosal Mast Cells ◽  
Mast Cell Heterogeneity

Increasing evidence for the existence of inter- and intra-species mast cell heterogeneity has expanded the potential biological role of this cell. Early studies suggesting that mast cells at mucosal sites differ morphologically and histochemically from connective tissue mast cells have been confirmed using isolated intestinal mucosal mast cells in the rat and more recently in man. These studies also established that mucosal mast cells are functionally distinct from connective tissue mast cells. Thus, mucosal and connective tissue mast cells differ in their responsiveness to a variety of mast cell secretagogues and antiallergic agents. Speculation about the therapeutic use of antiallergic drugs in disorders involving intestinal mast cells cannot, therefore, be based on extrapolation from studies of their effects on mast cells from other sites. Regulatory mechanisms for mast cell secretion may also be heterogeneous since mucosal mast cells differ from connective tissue mast cells in their response to a variety of physiologically occurring regulatory peptides. The development of techniques to purify isolated mast cell sub-populations will facilitate future analysis of the biochemical basis of the functional heterogeneity of mast cells.

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