Mechanisms Governing Anaphylaxis: Inflammatory Cells, Mediators, Endothelial Gap Junctions and Beyond

Autor: Debendra Pattanaik, Aaisha Haque, Guha Krishnaswamy, Samantha Minh Thy Nguyen, Chase Preston Rupprecht, Joseph S. Yusin
Rok vydání: 2021
Předmět:
0301 basic medicine
hypotension
Review
allergic reaction
Immunoglobulin E
chemistry.chemical_compound
0302 clinical medicine
complement
Biology (General)
Spectroscopy
biology
Degranulation
Gap Junctions
General Medicine
Mast cell
Computer Science Applications
Chemistry
medicine.anatomical_structure
Anaphylaxis
Histamine
QH301-705.5
tryptase
Tryptase
Basophil degranulation
Catalysis
Capillary Permeability
Inorganic Chemistry
03 medical and health sciences
anaphylaxis
medicine
Animals
Humans
epinephrine
coagulation
Physical and Theoretical Chemistry
QD1-999
Molecular Biology
Inflammation
food allergy
Platelet-activating factor
business.industry
angioedema
Organic Chemistry
anaphylactic shock
allergy
medicine.disease
histamine
cytokines
030104 developmental biology
030228 respiratory system
chemistry
Immunology
biology.protein
Endothelium
Vascular
mast cell
business
Zdroj: International Journal of Molecular Sciences
International Journal of Molecular Sciences, Vol 22, Iss 7785, p 7785 (2021)
ISSN: 1422-0067
DOI: 10.3390/ijms22157785
Popis: Anaphylaxis is a severe, acute, life-threatening multisystem allergic reaction resulting from the release of a plethora of mediators from mast cells culminating in serious respiratory, cardiovascular and mucocutaneous manifestations that can be fatal. Medications, foods, latex, exercise, hormones (progesterone), and clonal mast cell disorders may be responsible. More recently, novel syndromes such as delayed reactions to red meat and hereditary alpha tryptasemia have been described. Anaphylaxis manifests as sudden onset urticaria, pruritus, flushing, erythema, angioedema (lips, tongue, airways, periphery), myocardial dysfunction (hypovolemia, distributive or mixed shock and arrhythmias), rhinitis, wheezing and stridor. Vomiting, diarrhea, scrotal edema, uterine cramps, vaginal bleeding, urinary incontinence, dizziness, seizures, confusion, and syncope may occur. The traditional (or classical) pathway is mediated via T cells, Th2 cytokines (such as IL-4 and 5), B cell production of IgE and subsequent crosslinking of the high affinity IgE receptor (FcεRI) on mast cells and basophils by IgE-antigen complexes, culminating in mast cell and basophil degranulation. Degranulation results in the release of preformed mediators (histamine, heparin, tryptase, chymase, carboxypeptidase, cathepsin G and tumor necrosis factor alpha (TNF-α), and of de novo synthesized ones such as lipid mediators (cysteinyl leukotrienes), platelet activating factor (PAF), cytokines and growth factors such as vascular endothelial growth factor (VEGF). Of these, histamine, tryptase, cathepsin G, TNF-α, LTC4, PAF and VEGF can increase vascular permeability. Recent data suggest that mast cell-derived histamine and PAF can activate nitric oxide production from endothelium and set into motion a signaling cascade that leads to dilatation of blood vessels and dysfunction of the endothelial barrier. The latter, characterized by the opening of adherens junctions, leads to increased capillary permeability and fluid extravasation. These changes contribute to airway edema, hypovolemia, and distributive shock, with potentially fatal consequences. In this review, besides mechanisms (endotypes) underlying IgE-mediated anaphylaxis, we also provide a brief overview of IgG-, complement-, contact system-, cytokine- and mast cell-mediated reactions that can result in phenotypes resembling IgE-mediated anaphylaxis. Such classifications can lead the way to precision medicine approaches to the management of this complex disease.
Databáze: OpenAIRE
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