Dermal filler complications and management
Michael Parker, Charlie James in Fundamentals for Cosmetic Practice, 2022
Degranulation is, in essence, the release of said granular contents from within a cell to its surrounding environment. Regarding anaphylaxis, the mechanism of release is through a tyrosine-kinase phosphorylation cascade after a pro-inflammatory cell (such as a mast cell) has been activated by an IgE-antigen complex. The relevance of a phosphorylation cascade is that through enzymatic phosphorylation a small signal can be rapidly and significantly amplified via a short series of chemical reactions. This phosphorylation cascade results in an influx in intracellular calcium, which in itself is the trigger for degranulation to occur. When mast cells degranulate, they release pro-inflammatory mediators such as histamine, prostaglandin and cytokines such as TNF-α. See Figure 13.5.
Acute erythematous rash on the trunk and limbs
Richard Ashton, Barbara Leppard in Differential Diagnosis in Dermatology, 2021
Acute urticaria is defined as urticaria which has been present for less than 6 weeks. Individual lesions last for less than 24 hours (‘here today and gone tomorrow’). A central itchy white papule or plaque due to dermal oedema (weal) is surrounded by an erythematous flare. The lesions are variable in size and shape, and may be associated with swelling of the soft tissues of the eyelids, lips and tongue (angioedema, see p. 70). To identify how long the weals last, draw around one, and ask to see the patient the following day. Lesions which last for longer than 24 hours should be classified as urticarial dermatoses and require a biopsy for diagnosis. The weal is the result of degranulation of mast cells releasing histamine and other mediators of inflammation. Degranulation can be caused by allergic (IgE) and non-allergic stimuli.
Mast Cell Biology and Its Role in the Immediate Skin Contact Reactions
Ana M. Giménez-Arnau, Howard I. Maibach in Contact Urticaria Syndrome, 2014
The binding of monomeric IgE to FcεRI on skin MCs has a number of different and important effects, including the upregulation of FcεRI expression (i.e., an increase in FcεRI numbers on skin MC membranes). The reason for this is that IgE stabilizes FcεRI by binding to its a-chain, which inhibits FcεRI internalization and degradation. Monomeric IgE also increases FcεRI production and shuttling to the MC membrane. Importantly, the binding of IgE to FcεRI can also result in the production of cytokines. In addition, monomeric IgE can promote MC differentiation and increase MC responses to activating signals. The binding of monomeric IgE does not result in MC degranulation. For this, FcεRI cross-linking is required (i.e. two or more FcεRIs need to dimer-ize to induce degranulation). The extent of MC degranulation is linked to the number of FcεRIs cross-linked. In other words, the higher the numbers of FcεRIs that aggregate on the membrane of MCs, the higher the number of MC granules released. Skin MCs express several thousands to hundreds of thousands FcεRIs under physiological conditions. Aggregation of as few as a couple of hundred FcεRIs is sufficient to induce MC degranulation.[2,3,9]
Inhibitory activity of narirutin on RBL-2H3 cells degranulation
Published in Immunopharmacology and Immunotoxicology, 2021
Liyan Niu, Jihao Wei, Xuwen Li, Yongri Jin, Xiaolei Shi
As shown in Figure 3, single cell topography looked like a shuttle in A1 and A3, but that of A2 looked like a sphere and it was brighter than A1. C2 had a much stronger stereo feeling than C1 and C3 in their 3 D topographical image. These results demonstrated that narirutin had a positive effect on stabilizing morphology of activated cells. Small holes can be observed on cell membrane of B1 and B3 obviously, in contrast, the membrane projection and holes approximately disappearing were observed in B2 cells. Muchmore, B2 cells were surrounded by more prominent unknown vesicles and granular material. That is just the fact that cell degranulation may be a process of exocytosis. In other words, there are many particles stored in cells that would be released when cells were stimulated, these vesicles from the cytoplasm to outside the membrane. More importantly, as shown in the curve, vesicles of sensitized RBL-2H3 cells had a higher height as comparing with other groups. These results showed that DNP-BSA can promote sensitized RBL-2H3 cells transfer more vesicles to the edge and supernatant of RBL-2H3 cells, and lead to cell more granules release. However, narirutin could suppress this phenomenon in a certain extent.
Carbonic anhydrase enzymes for regulating mast cell hematopoiesis and type-2 inflammation: a patent evaluation (WO2017/058370)
Published in Expert Opinion on Therapeutic Patents, 2018
Jean-Yves Winum
Potential implications of CA in inflammation and its role in mast cells are poorly documented in literature. Mast cells are regulatory hematopoietic cells essential for the modulation of inflammatory and allergic processes. Together with dendritic cells and monocytes, they constitute the first line of defense against antigens such as bacteria or parasites. They also play a role in reactions to environmental allergens. The main mechanism of activation of mast cells lies in the binding between the antigen and the IgE bound to their membrane and originating from the B lymphocytes, triggering an intracellular activating cascade. Mast cells can also be activated by detecting cytokines or antigens via specific receptors on their surface. Once activated, mast cells release preformed granules into their environment and contain them in their cytoplasm. This process is called degranulation. These granules contain immuno-reactive mediators such as heparin or histamine, whose function is to promote the inflammatory process and eliminate the pathogen. Mast cells are also capable of producing other substances such as lipid mediators, cytokines, or chemokines that participate in signaling and cellular communication to coordinate the innate and adaptive immune responses [8–11].
Evidence-based indications of platelet-rich plasma therapy
Published in Expert Review of Hematology, 2021
Shyla Gupta, Anna Paliczak, Diego Delgado
The overarching process of preparing PRP begins with collecting blood and the combination of an anticoagulant factor. Research regarding specific anticoagulant factors such as anticoagulated whole blood, and citrate-anticoagulated whole blood is still uncertain [8]. This process happens before centrifugation. The preparation differentiates red blood cells from platelet-poor plasma and what is known as the ‘buffy coat.’ The buffy coat is composed of concentrated platelets and leukocytes [31]. Platelets are segregated using differing methodologies and can be activated through amalgamation with calcium chloride or thrombin. These two activating agents are specific compounds that cause a degranulation reaction to release growth factors [32]. Platelet activation is correlated with a release of a wide range of chemokines and pro-inflammatory lipids that induce specific effects on a large variety of tissues and cells, including leukocytes [33]. Specifically, during thrombosis, leukocytes’ release is considered an important step that links thrombosis to inflammatory responses and increases the procoagulant state. This event is strictly controlled and affected by the delicate interactions between cells at the site of injury. The relationship between platelets and leukocytes corresponds with a vast array of mediators, including adhesion molecules, chemokines, proteins, and various pro-inflammatory lipids [33].
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