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DIFFERENT SIGNALS INDUCE MAST CELL INFLAMMATORY ACTIVITY: INHIBITORY EFFECT OF VITAMIN E
No full textVitamin supplementation in disease reduces morbidity and mortality in humans by promoting the activation of different genes which influence several pathways. The purpose of this article is to clarify the role of vitamin E in mast cell inflammation. Vitamin E is a fat soluble antioxidant which protects from low-density lipoprotein (LDL) oxidation. Vitamin E promotes a barrier function and anti-inflammatory responses by binding the regulatory domain of protein kinase C alpha (PKC alpha) (a regulator and antagonist of heart failure) and decreases the activation of NF-kappa B, a proinflammatory transcription factor, causing the generation of cytokines/chemokines and mast cell activation. Mast cells participate in innate and acquired immunity and inflammation. Several factors, including cytokines and chemokines, regulate the development and migration of activated mast cells. Mast cells generate and release inflammatory compounds in asthma and allergic diseases and have a detrimental effect on the vessel wall, which can be inhibited by vitamin E. Vitamin E inhibits histamine release generated in activated mast cells, increases calcium Ca2+ uptake and prevents the oxidation of unsaturated fatty acids. Vitamin E is relatively non-toxic, however, administered at very high doses may suppress normal hematological response as well as causing other adverse effects. Therefore, vitamin E may be beneficial in the prevention of diseases mediated by mast cells and can have special value in the treatment of asthma and allergic diseases; however, the exact mechanism by which vitamin E acts is still unclear, thus warranting future research
Anaphylaxis is a rare reaction in COVID-19 vaccination
No full text: Anaphylaxis is a severe multisystem reaction that occurs rapidly after the introduction of an antigen that would otherwise be a harmless substance. It is characterized by airway and respiratory problems, cardiovascular collapse, mucosal inflammation, and other complications, all severe symptoms that can cause death. IgE-dependent anaphylaxis involves mast cells (MCs) which are the main sources of biologically active mediators that contribute to the pathological and lethal phenomena that can occur in anaphylaxis. Antibody-mediated anaphylaxis can follow multiple pathways such as that mediated by MCs carrying the FcεRI receptor, which can be activated by very small amounts of antigen including a vaccine antigen and trigger an anaphylactic reaction. In addition, anaphylaxis can also be provoked by high concentrations of IgG antibodies that bind to the FcγR receptor present on basophils, neutrophils, macrophages and MCs. For this reason, the IgG concentration should be kept under control in vaccinations. Activation of MCs is a major cause of anaphylaxis, which requires immediate treatment with epinephrine to arrest severe lethal symptoms. MCs are activated through the antigen binding and cross-linking of IgE with release of mediators such as histamine, proteases, prostaglandins, leukotrienes and inflammatory cytokines. The release of these compounds causes nausea, vomiting, hives, wheezing, flushing, tachycardia, hypotension, laryngeal edema, and cardiovascular collapse. mRNA and viral vector vaccines have been cleared by the United States, Food and Drug Administration (FDA), generating hope of prevention and cure for COVID-19 around the world. Scientists advise against giving the vaccine to individuals who have had a previous history of anaphylaxis. The US Centers for Disease Control and Prevention (CDC) advises people with a previous history of any immediate allergic reaction to remain under observation for approximately 30 minutes after COVID-19 vaccination. To date, vaccines that prevent SARS-CoV-2 infection have not raised major concerns of severe allergic reactions, although, in some cases, pain and redness at the injection site and fever have occurred after administration of the vaccine. These reactions occur in the first 24-48 hours after vaccination. It has been reported that probable forms of anaphylaxis could also occur, especially in women approximately 40 years of age. But after tens of millions of vaccinations, only a few patients had this severe reaction with a low incidence. Anaphylactic and severe allergic reactions can also occur to any component of the vaccine including polysorbates and polyethylene glycol. To date, there is no precise information on allergic reactions to COVID-19 vaccines. Individuals with MCs and complement with higher activation than others may be at greater allergic risk. Moreover, the reactions called anaphylactoids, are those not mediated by IgE because they do not involve this antibody and can also occur in COVID-19 vaccination. These not-IgE-mediated reactions occur through direct activation of MCs and complement with tryptase production, but to a lesser extent than IgE-mediated anaphylaxis. However, at the moment it is not known exactly which component of the vaccine causes the allergic reaction and which vaccine causes the most side effects, including anaphylaxis. Thus, individuals who have a known allergy to any component of the vaccine should not be vaccinated. However, should an anaphylactic reaction occur, this requires immediate treatment with epinephrine to arrest severe lethal symptoms. In conclusion, the purpose of this editorial is to encourage the population to be vaccinated in order to extinguish this global pandemic that is afflicting the world population, and to reassure individuals that anaphylactic reactions do not occur with a higher incidence than other vaccinations
CAR-T cell therapy causes inflammation by IL-1 which activates inflammatory cytokine mast cells: anti-inflammatory role of IL-37
No full textChimeric antigen receptor (CAR) T cells are genetically modified T cells that act against cancer. When CAR-T cells are administered they can trigger inflammatory cytokines and increase toxicity. Interleukin (IL)-1 is the classic cytokine that mediates inflammatory reactions including those that occur in CAR-T-cell therapy. IL-1 also induces IL-33 in mast cells (MCs), amplifying the allergic reaction. IL- 37 (ILF7) is an IL-1 family member which binds IL-18 receptor alpha (IL-18Rα) chain and suppresses innate and acquired immunity. IL-37 is an anti-inflammatory cytokine which inhibits pro-inflammatory cytokines including IL-1 and IL-33. Here, we hypothesize that inflammation and toxicity generated in tumor CAR-T therapy could be inhibited by IL-37, contributing to an improvement in the treatment of tumors with CAR-T therapy
Mast cell virus infection and inflammatory cytokines
No full textMast cells (MCs) are hematopoietic cells developed from bone marrow progenitors in response to the ligand stem cell factor, a trans-membrane tyrosine kinase kit receptor. MCs are located virtually in all vascularized tissues and in proximity to neurons and play a decisive role in both innate and adaptive immune responses. Their activation is involved in oxidative stress correlated with infection and inflammation. Pro-inflammatory cytokines are secreted by MCs after physiologic and psychological stress due to virus infection, including SARS-CoV-2. MCs, along with macrophages and pulmonary alveolar epithelial cells, are the main targets attacked by the coronavirus. COVID-19 induced by SARS-CoV-2
causes inflammatory stress which activates MCs to secrete corticotrophin-releasing hormone (CRH), SP, IL-6, TNF, and IL-1. Toll-like receptor (TLR) virus activation in MCs leads to pro-inflammatory cytokine generation without degranulation, an effect that can be inhibited by IL-10, IL-4, IL-1Ra and IL-37.
TLR has the ability to recognize extracellular PAMPs by causing the transcription of NLRP, pro-IL-1, and other pro-inflammatory cytokines. The multi-protein complex, comprising pro-caspase-1, activates caspase-1 which in turn activates pro-IL-1 that is transformed into highly inflammatory mature IL-1.
In COVID-19, viral RNA is specifically recognized by TLR, followed by recruiting the signal transfer proteins MyD88, IRAK, IKK and TRAF6 which can activate the NF-κB, resulting in transcription of the pro-inflammatory cytokines IL-1 and TNF, responsible for the “cytokine storm” phenomenon.
Meanwhile, a new variant of the coronavirus-19 called C.1.2. has been discovered in the United States in the past few days, the effects of which are unknown, and it is therefore of great concern. Researchers are now testing it on immune cells to see if they react and are comparing it to a delta variant. Thus, from
the existing data in biomedical literature, we can conclude that the suppression of pro-inflammatory cytokines in viral infections (including COVID-19) mediated by MCs represents a promising therapy not only in this field of medicine, but also in autoimmune, allergic, and cardiovascular disorders, as well as tumor inflammation where MCs play a key role
Induction of pro-inflammatory cytokines (IL-1 and IL-6) and lung inflammation by COVID-19: anti-inflammatory strategies
No full textCoronavirus-19 (COVI-19) involves humans as well as animals and may cause serious damage to the respiratory tract, including the lung: coronavirus disease (COVID-19). This pathogenic virus has been identified in swabs performed on the throat and nose of patients who suffer from or are suspected of the disease. When COVI-19 infect the upper and lower respiratory tract it can cause mild or highly acute respiratory syndrome with consequent release of pro-inflammatory cytokines, including interleukin (IL)-1β and IL-6. The binding of COVI-19 to the Toll Like Receptor (TLR) causes the release of pro-IL-1β which is cleaved by caspase-1, followed by inflammasome activation and production of active mature IL-1β which is a mediator of lung inflammation, fever and fibrosis. Suppression of pro-inflammatory IL-1 family members and IL-6 have been shown to have a therapeutic effect in many inflammatory diseases, including viral infections. Cytokine IL-37 has the ability to suppress innate and acquired immune response and also has the capacity to inhibit inflammation by acting on IL-18Rα receptor. IL-37 performs its immunosuppressive activity by acting on mTOR and increasing the adenosine monophosphate (AMP) kinase. This cytokine inhibits class II histocompatibility complex (MHC) molecules and inflammation in inflammatory diseases by suppressing MyD88 and subsequently IL-1β, IL-6, TNF and CCL2. The suppression of IL-1β by IL-37 in inflammatory state induced by coronavirus-19 can have a new therapeutic effect previously unknown. Another inhibitory cytokine is IL-38, the newest cytokine of the IL-1 family members, produced by several immune cells including B cells and macrophages. IL-38 is also a suppressor cytokine which inhibits IL-1β and other pro-inflammatory IL-family members. IL-38 is a potential therapeutic cytokine which inhibits inflammation in viral infections including that caused by coronavirus-19, providing a new relevant strategy
Impact of mast cells in systemic lupus erythematosus: can inflammation be inhibited?
No full text: Systemic lupus erythematosus (SLE), is a complex chronic inflammatory autoimmune disease, with rheumatological manifestations, which afflicts mainly women. SLE presents various heterogeneous clinical aspects and different pathogeneses and involves the production of anti- DNA autoantibodies which are deposited as immune complexes in various organs and tissues, provoking inflammation. These diseases cause multiple tissue and organ damage in arthritis, skin lesions, hematologic changes, renal and neurologic disorders, and others (Table I). In SLE, serum contains anti-nucleus antibodies and anti-DNA antibodies that can be important biomarkers for patients suffering from this disease
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Mast cells and virus
No full textMast cells (MCs) are hematopoietic cells that reside ubiquitously in all vascularized tissues. They are potential sources of a wide variety of biologically active secreted compounds, including diverse cytokines, chemokines and growth factors. In addition, they participate in innate and adaptive immune responses. MCs are the most important cells in immediate reactions and chronic IgE-associated allergic disorders and enhance the host resistance to certain biological agents, including viruses. Therefore, MCs influence many biological responses to viruses and other microbiological agents. Viruses activate MCs through TLR4 leading to the generation of several pro-inflammatory cytokines, including those of the IL-1 family. Here, we report how viruses can activate MCs producing severe inflammation and how these interesting cells can activate the immune system by carrying out a protective action for our organism
IL-33 mediates allergy through mast cell activation: Potential inhibitory effect of certain cytokines
No full textMast cells (MCs) are hematopoietic immune cells commonly found in adjacent to blood vessels in the lamina propria of airway mucosa. They are important in allergic reactions since the cross-linking of their surface high affinity receptor FceRI induces activation of these cells, and provokes the synthesis, degranulation and release of inflammatory mediators including arachidonic acid-derived eicosanoids (de novo synthesized), stored enzyme mediators, and inflammatory TH1 and TH2 cytokines, and chemokines. Interleukin (IL)-33 participates in innate and adaptive immunity and inflammation and, acting on CD34+ cells, causes MC differentiation and maturation. IL-33 is generated by activated immune cells, and activates MCs which degranulate and release pro-inflammatory mediators. IL-33 is very important in mediating allergic inflammation and can be induced by IL-1 beta. It is also called “alarmin” and is an inflammatory cytokine IL-1 family member, expressed from mocytes and MCs, which binds its receptor ST2, provoking its release after cell damage. MC-derived allergic compounds in response to IL-33 is critical to innate type 2 immunity. IL-37 is expressed by immune and non-immune cells after pro-inflammatory stimulus. IL-37, an anti-inflammatory cytokine, binds IL-18Ra and suppresses pro-inflammatory IL-1 beta released by activated immune cells such as macrophages. Here, we hypothesize that pro-inflammatory IL-1 family member cytokines released by activated MCs, mediating inflammatory allergic phenomenon, can be suppressed by IL-37
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