Mast cells as protectors of health
"Mast cells (MCs), which are well known for their effector functions in TH2-skewed allergic and also autoimmune inflammation, have become increasingly acknowledged for their role in protection of health. It is now clear that they are also key modulators of immune responses at interface organs, such as the skin or gut. MCs can prime tissues for adequate inflammatory responses and cooperate with dendritic cells in T-cell activation. They also regulate harmful immune responses in trauma and help to successfully orchestrate pregnancy. This review focuses on the beneficial effects of MCs on tissue homeostasis and elimination of toxins or venoms. MCs can enhance pathogen clearance in many bacterial, viral, and parasitic infections, such as through Toll-like receptor 2ātriggered degranulation, secretion of antimicrobial cathelicidins, neutrophil recruitment, or provision of extracellular DNA traps. "
Anne Dudeck, PhD, et.al.
https://www.jacionline.org/article/S0091-6749(18)31605-1/pdf
Innate Immunity Induces the Accumulation of Lung Mast Cells During Influenza Infection
Behdad Zarnegar, et.al
"Mast cells release disease-causing mediators and accumulate in the lung of asthmatics. The most common cause of exacerbations of asthma is respiratory virus infections such as influenza.
Recently, we demonstrated that influenza infection in mice triggers the recruitment of mast cell progenitors to the lung. This process starts early after infection and leads to the accumulation of mast cells.
Previous studies showed that an adaptive immune response was required to trigger the recruitment of mast cell progenitors to the lung in a mouse model of allergic lung inflammation.
Therefore, we set out to determine whether an adaptive immune response against the virus is needed to cause the influenza-induced recruitment of mast cell progenitors to the lung."
Inflammatory Response of Mast Cells during Influenza A Virus Infection Is Mediated by Active Infection and RIG-I Signaling
Amy C. Graham
Cytokine Storm Syndrome Looking Toward the Precision Medicine Era Edward
M. Behrens and Gary A. Koretzky
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From my Doctorās Allergy Partners post.
The Circadian Clock Drives Mast Cell Functions in Allergic Reactions
Pia Christ, Anna Sergeevna Sowa, [ā¦], and Axel Lorentz
"Allergic conditions such as asthma or allergic rhinitis have historically shown circadian bias as the severity of symptoms is exacerbated between midnight and morning time and exhibits prominent 24-h variation (12, 13).
Mast cells are known to have multiple immunoregulatory functions through the release of their mediators, such as histamine, leukotrienes, cytokines, chemokines and proteases and also serve as the key drivers of long-term pathophysiological changes associated with chronic allergic responses (14, 15).
Mast cell activation occurs during type I allergic reactions via antigen-mediated aggregation of immunoglobulin E-bound FcĪµRIs (Figure ā(Figure1)1) (16, 17).
As they are the main effector cells in allergy, the rhythmicity of mast cells has also come under investigation.
For example, in some of the earlier findings, serum mast cell tryptase and plasma histamine levels were shown to be lower in the afternoon but peaked during night (18, 19).
In the following review, we give a brief overview of the role of the circadian clock in regulating mast cells and allergic reactions. As there are various types of mast cells (20), it is conceivable to think that the circadian clock regulates the expression of type-specific genes leading to different functions."
A circadian based inflammatory response ā implications for respiratory disease and treatment
Maria Comas, Christopher J. Gordon,
Craig L. Phillips, et.al
"The greatest response of the immune system in terms of cytokine release occurs during the rest and early active periods.
However, this also implies that the risk of immune-related illnesses, such as, sepsis, allergies and uncontrolled immune reactions are more likely to occur during the late rest period and early active period.
Allergic reactions are initiated with antigen specific IgE production and fixation of IgE to FcĪµRI receptors on mast cells and basophils (Stone et al. 2010).
Importantly mast cells, eosinophils and basophils display circadian oscillations of clock gene expression as well as circadian gene expression and release of their mediators following IgE-mediated activation (Baumann et al. 2013; Wang et al. 2011; Ando et al. 2015; Baumann et al. 2015).
Several recent studies have shown that the circadian clock regulated the daily rhythms in IgE/mast cell-mediated allergic reactions."
Excellent review
IgE, mast cells, basophils, and eosinophils
Kelly D. Stone, MD, PhD, Calman Prussin, MD, and Dean D. Metcalfe, MD Bethesda, Md
"IgE, mast cells, basophils, and eosinophils are essential components of allergic inflammation. Antigen-specific IgE production, with subsequent fixation of IgE to FceRI receptors on mast cells and basophils, is central to the initiation and propagation ofimmediate hypersensitivity reactions. Mast cells, basophils, and eosinophils are central effector cells in allergic inflammation, as well as in innate and adaptive immunity. This review highlights what is known about these components and their roles in disease pathogenesis. (J Allergy Clin Immunol 2010;125:S73-80.)
https://www.jacionline.org/article/S0091-6749(09)01734-5/pdf
Histamine: neural circuits and new medications
Thomas E Scammell
"Most research has focused on the TMN as a key source of histamine, but microglia can produce histamine in response to lipopolysaccharide [38], and about half of all brain histamine is produced by mast cells, which are scattered across the brain [39].
Asthma and allergic rhinitis are often worst at night, and the molecular circadian clock regulates the reactivity of mast cells in the periphery [40].
Much less is known about mast cells in the brain and what may trigger them to release histamine. One study found that activation of brain mast cells can increase wakefulness, and the sedating effects of selective H1 receptor antagonists such as tiprolidine are absent in mice lacking mast cells [41].
Mice normally show a strong increase in wake when food deprived, but mice without mast cells lack this response, either due to poor promotion of wake or reduced appetite [41].
In addition, chronic mild stress doubles the number of brain mast cells and increases wake during the active period [42].
Although these observations are intriguing, mice lacking mast cells have normal amounts of wake, NREM, and REM sleep [41], and determining how these cells contribute to normal or pathological sleep/wake behavior will be important directions for future research."
Beans, Beans maybe not so good for the heartā¦
Histamine releases in addition to fartsā¦
Lectin is the issue, so hereās the dealā¦
Check with your doctor before having beans at every mealā¦
Do dietary lectins cause disease?
The evidence is suggestiveāand raises interesting possibilities for treatment
David L J Freed, Allergist
"Among the effects observed in the small intestine of lectin fed rodents is stripping away of the mucous coat to expose naked mucosa and overgrowth of the mucosa by abnormal bacteria and protozoa.14
Lectins also cause discharge of histamine from gastric mast cells,15 which stimulates acid secretion.
So the three main pathogenic factors for peptic ulcerāacid stimulation, failure of the mucous defence layer, and abnormal bacterial proliferation (Helicobacter pylori) are all theoretically linked to lectins. "
Potato lectin activates basophils and mast cells of atopic subjects by its interaction with core chitobiose of cell-bound non-specific immunoglobulin E
S N Pramod, Y P Venkatesh, and P A Mahesh
"A major factor in non-allergic food hypersensitivity could be the interaction of dietary lectins with mast cells and basophils.
Because immunoglobulin E (IgE) contains 10ā12% carbohydrates, lectins can activate and degranulate these cells by cross-linking the glycans of cell-bound IgE.
The present objective focuses on the effect of potato lectin (Solanum tuberosum agglutinin; STA) for its ability to release histamine from basophils in vitro and mast cells in vivo from non-atopic and atopic subjects. "
Regulation of Immune and Nonimmune Mast Cell Activation by Phenols from Olive Oil
By Alicia Beatriz Penissi
āThe purpose of this study is to establish if hydroxytyrosol and oleuropein, the most significant phenols found in olive oil and olives, can inhibit the activation of mast cells induced by immune and nonimmune pathways.ā
"Mast cells may be activated via several different mechanisms, among which is the classical pathway known as immunological or IgE-mediated mast cell activation, triggered by the cross-linking of FcĪµRI receptors.
Mast cell activation may also be completed in an IgE-independent manner using commercially available activators, such as basic secretagogues and calcium ionophores.
Concanavalin A is a glucose-/mannose-specific lectin that activates mast cells by a mechanism similar to the antigen-antibody reaction. This lectin causes FcĪµRI receptors to cluster on cell membranes. In turn, this triggers a series of intracellular events leading to the secretion of mast cell mediators by exocytosis"
"Our present findings reveal for the first time that hydroxytyrosol and oleuropein, the major phenolic compounds in olive, inhibit mast cell degranulation triggered by both immune and nonimmune pathways. Our discoveries also suggest that olive polyphenols, especially hydroxytyrosol and oleuropein, may provide insights to develop useful tools to prevent and treat mast cell-mediated disorders. "
https://www.intechopen.com/books/technological-innovation-in-the-olive-oil-production-chain/regulation-of-immune-and-nonimmune-mast-cell-activation-by-phenols-from-olive-oil
How mast cells make decisions
Jƶrn Karhausen1 and Soman N. Abraham
āSpecifically, the authors carefully compared degranulation and mediator responses in MCs that had been activated via the classical FcĪµRI receptor or the recently described G proteinācoupled receptor (GPCR) MRGPRX2 (or its murine ortholog MRGPRB2), which binds various cationic ligands, such as substance P (SP), and is almost exclusively found on MCs (11). While activation of either pathway elicited a comparable degranulation response, FcĪµRI stimulation triggered greater release of prostaglandin E2 (PGE2), cytokines, and VEGF. In MRGPRX2-stimulated cells, the PGE2 response was limited and no VEGF was detected. In addition, FcĪµRI-mediated degranulation was linked to a slower but sustained Ca2+ response, whereas MRGPRX2-mediated degranulation was very rapid, with a transient Ca2+ response (10). Because Ca2+ signaling is critical for MC degranulation, it is not surprising that each receptor evoked distinct degranulation dynamics. Moreover, FcĪµRI-mediated degranulation involved initial fusion events between granules followed by the emergence of complex granules that were present as large and nonspherical particles in a limited number of openings. The misshapen appearance of granules in MCs undergoing FcĪµRI-mediated exocytosis is presumed to be the result of the initial granule fusion events. Conversely, MRGPRX2-triggered degranulation was characterized by direct release of individual, spherical granules from all over the MC surface.ā