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Anaphylaxis
Published in Pudupakkam K Vedanthan, Harold S Nelson, Shripad N Agashe, PA Mahesh, Rohit Katial, Textbook of Allergy for the Clinician, 2021
IgE is bound to high-affinity receptor FcƐRI on the surfaces of blood basophils and tissue mast cells. In the classic IgE-mediated allergic reaction, a circulating allergen interacts with surface-bound FcƐRIIgE, cross-links two IgE molecules on the mast cell or basophil. This in turn initiates intracellular signaling for the cell to degranulate and release preformed mediators, enzymes, and cytokines as well as induces de novo synthesis of inflammatory mediators (Reber et al. 2017). These chemical mediators act directly on tissues and result in the previously described allergic symptoms. Figures 22.1 and 22.2 demonstrate mediators of anapyhylaxis and their tissue targets, resulting in anaphylaxis symptoms (Reber et al. 2017, Castells 2017). Additional inflammatory cells, in particular eosinophils, are recruited and stimulated to release additional chemical mediators. This results in full-blown allergic inflammation and the clinical signs of anaphylaxis.
In Vivo Models of Smooth Muscle Growth
Published in Alastair G. Stewart, AIRWAY WALL REMODELLING in ASTHMA, 2020
A number of potentially interesting candidate growth-promoting substances have been identified by in vitro testing. Of particular interest are those associated with allergic inflammation since allergy is one of the best-characterised mechanisms by which asthma is induced. Thromboxane, endothelin, cysteinyl-leukotrienes, and histamine have been shown to have mitogenic activity.24–26 The evidence for the synthesis and release of these substances in asthma is solid. The precise mechanisms by which such bronchoconstrictive mediators stimulate smooth muscle proliferation in vitro appear to be complex and to involve interactions among them. For example, endothelin causes phospholipase A2 activation and thromboxane synthesis in cultured rabbit airway smooth muscle cells. Thromboxane, in turn, triggers cysteinyl-leukotriene synthesis.24 The mitogenic activity of endothelin seems to mediated by leukotriene and so is indirect.
Platelet-Activating Factor Receptors in the Airways
Published in Devendra K. Agrawal, Robert G. Townley, Inflammatory Cells and Mediators in Bronchial Asthma, 2020
Several lines of evidence suggest that T-lymphocytes and their soluble products regulate the cellular components of allergic inflammation in the late-phase allergic reaction.122 Deficiency of concanavalin A-induced suppressor cell function in asthmatic subjects has been observed by a number of investigators.201–203 Very recently, Frew and colleagues204 have demonstrated significant infiltration by CD3+/CD4+ T-lymphocytes together with evidence of T-cell activation in the allergen-induced late-phase skin reaction in human atopic subjects. It is therefore possible that T-cell products may influence the allergic response by interacting with other inflammatory cells such as eosinophils. In fact, Gerblich and colleagues205 have demonstrated a selective loss of circulating helper (OKT4) T-cells and an apparent increase in activated (Ia positive) T-cells after antigen-induced asthma. There was a good correlation between these changes and blood eosinophilia. This suggests the activation of T-cells and the concomitant release of the eosinophil-stimulating substances.
Updates in the diagnosis and practical management of allergic rhinitis
Published in Expert Review of Clinical Pharmacology, 2023
Chiara Trincianti, Maria Angela Tosca, Giorgio Ciprandi
Allergic rhinitis is the most frequent IgE-mediated disease and recognizes a type 2 phenotype characterized by eosinophilic infiltrate and allergen exposure-dependent inflammation [68]. Although it is well known, and several guidelines have established precise diagnostic criteria and treatment protocols, controlling allergic rhinitis is not optimal in most patients [69]. In this regard, an attracting issue concerns the availability of simple biomarkers measuring type 2 inflammation. That is, it is well known that allergic inflammation may be present despite symptoms, such as the concept of minimal persistent inflammation [70]. In other words, the possibility of documenting the presence and severity of type 2 inflammation can modulate the use of antiallergic treatments. In fact, patients prefer to take drugs on demand, but this approach could be inappropriate, mainly if inflammation persists also without overt symptoms. In this regard, a trivial blood cell count is recommended for getting a rough idea of the degree of type 2 inflammation [71]. However, it remains desirable to also have biomarkers that can predict the response to AIT and define the efficacy so that treatment can be discontinued judiciously.
Allergen immunotherapy: progress and future outlook
Published in Expert Review of Clinical Immunology, 2023
Lara Šošić, Marta Paolucci, Stephan Flory, Fadi Jebbawi, Thomas M. Kündig, Pål Johansen
Allergic inflammation can be classified as a hypersensitivity reaction to environmental antigens according to Coombs and Gell [28], orchestrated by IgE antibodies (type-1-hypersensitivity reaction) or T cells (type-4-hypersensitivity reaction); type 2 and type 3 reactions are orchestrated by IgG or IgM antibodies or by immune complexes that also involve immune complexes. IgE-dependent allergies are also called immediate-type allergic reactions, or anaphylactic hypersensitivity reactions, as the onset is generally in the first minutes after exposure [29]. Examples of immediate-type allergic reactions include allergic rhinoconjunctivitis (ARC), allergic asthma, and anaphylaxis. Type 4 or delayed-type allergic reactions, e.g. contact dermatitis (CD), can manifest several days after exposure, and is not to be confused with the late-phase, but IgE-mediated type-1 allergic reaction that can occur several hours after allergen exposure due to release of additional mediators from mast cells and basophils [29].
A RAS inhibitor reduces allergic airway remodeling via regulating IL-33-derived type 2 innate lymphoid cells
Published in Experimental Lung Research, 2021
Toshifumi Tezuka, Masahiko Azuma, Hirohisa Ogawa, Mayo Kondo, Hisanori Uehara, Yoshinori Aono, Masaki Hanibuchi, Yasuhiko Nishioka
A major limitation of this study is the use of selective but unspecific chemical inhibitors. Recently, molecular targeted drugs such as anti-IgE antibody, anti-IL4R antibody, anti-IL5 antibody and anit-IL-5R antibody, have been clinically applied for the treatment of bronchial asthma, and shown to be useful and specific. XRP44X selectively inhibits the RAS-ERK pathway, but also inhibits cytoskeletal polymerization, and its target are not specific to allergic airway inflammation or remodeling.23 When considered in clinical practice, it may cause adverse events by suppressing the function of maintaining homeostasis of cells that are not involved in allergic inflammation or remodeling such as repair and infection protection.23 In this respect, clinical application may be limited at present. This study shows that suppressing the RAS-ERK pathway and reducing the function of Th2 and ILC2 is a reasonable approach to suppress allergic inflammation and remodeling. Further researches including improvement of drug delivery systems are needed to achieve clinical application.