Molecular Mechanisms in Anaphylaxis

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Immunology and Immunotherapy".

Deadline for manuscript submissions: closed (30 December 2022) | Viewed by 4462

Special Issue Editor


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Guest Editor
1. Department of Allergy and Immunology, IIS-Fundación Jiménez Díaz, UAM, 28040 Madrid, Spain
2. Faculty of Medicine and Biomedicine, Alfonso X El Sabio University, 28691 Madrid, Spain
Interests: anaphylaxis; immunology; vascular permeability; endothelium; molecular mechanisms; extracellular vesicles; miRNAs

Special Issue Information

Dear Colleagues,

Anaphylaxis (AX) is the most severe manifestation of allergic disorders, being a systemic hypersensitivity life-threatening reaction that evolves rapidly. Among the most frequent triggers are food, drugs, and hymenoptera venoms. The plethora of features associated with AX confers difficulties in its diagnosis, impairing the ability to adequately treat these severe reactions. Generally, the diagnosis is carried out according to the clinical symptoms, which are common to many other pathologies, so confirmation through in vitro markers and knowledge about their molecular mechanisms is advisable. Mast cells and basophils are recognized as effector cells eliciting the anaphylactic reaction. However, many other cells and mediators are also relevant. Moreover, the release of mediators causes an endothelial barrier breakdown. This fact produces an increase in vascular permeability and a leakage of fluids, which have influence in two decisive and severe factors (hypotension and hypoxia). Thus, the primary purpose of this Special Issue is to collect scientific contributions providing novel insight into the molecular mechanisms of AX.

Dr. Vanesa Esteban
Guest Editor

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Keywords

  • anaphylaxis
  • molecular mechanisms
  • mast cells
  • vascular permeability
  • food and drug allergies

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Published Papers (2 papers)

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Research

12 pages, 1823 KiB  
Article
The Hypertensive Effect of Amphotericin B-Containing Liposomes (Abelcet) in Mice: Dissecting the Roles of C3a and C5a Anaphylatoxins, Macrophages and Thromboxane
by Erik Őrfi, László Hricisák, László Dézsi, Péter Hamar, Zoltán Benyó, János Szebeni and Gábor Szénási
Biomedicines 2022, 10(7), 1764; https://doi.org/10.3390/biomedicines10071764 - 21 Jul 2022
Cited by 1 | Viewed by 1840
Abstract
Liposomal amphotericin B (Abelcet) can cause infusion (anaphylactoid) reactions in patients whose mechanism is poorly understood. Here, we used mice to investigate the role of complement (C) receptors and the cellular sources of vasoactive mediators in these reactions. Anesthetized male NMRI and thromboxane [...] Read more.
Liposomal amphotericin B (Abelcet) can cause infusion (anaphylactoid) reactions in patients whose mechanism is poorly understood. Here, we used mice to investigate the role of complement (C) receptors and the cellular sources of vasoactive mediators in these reactions. Anesthetized male NMRI and thromboxane prostanoid receptor (TP) or cyclooxygenase-1 (COX-1)-deficient and wild type C57Bl6/N mice were intravenously injected with Abelcet at 30 mg/kg. Mean arterial blood pressure (MABP) and heart rate (HR) were measured. In untreated mice, Abelcet caused a short (15 min) but large (30%) increase in MABP. C depletion with cobra venom factor (CVF) and inhibition of C5a receptors with DF2593A considerably prolonged, while C3aR inhibition with SB290157 significantly decreased the hypertensive effect. Likewise, the hypertensive response was abolished in COX-1- and TP-deficient mice. CVF caused a late hypertension in TP-deficient mice. Both macrophage depletion with liposomal clodronate and blockade of platelet GPIIb/IIIa receptors with eptifibatide prolonged the hypertensive effect. The early phase of the hypertensive effect is COX-1- and TP-receptor-dependent, partly mediated by C3aR. In contrast, the late phase is under the control of vasoactive mediators released from platelets and macrophages subsequent to complement activation and C5a binding to its receptor. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Anaphylaxis)
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10 pages, 1384 KiB  
Article
Characterization of Mast Cells from Healthy and Varicose Human Saphenous Vein
by Katrine T. Callesen, Sofia Mogren, Frida Berlin, Cecilia Andersson, Susanne Schmidt, Lotte Klitfod, Vanesa Esteban, Lars K. Poulsen and Bettina M. Jensen
Biomedicines 2022, 10(5), 1062; https://doi.org/10.3390/biomedicines10051062 - 3 May 2022
Cited by 2 | Viewed by 1871
Abstract
Mast cells (MCs) are distributed in tissues throughout the body and are highly involved in many physiological and pathophysiological processes. The potential and involvement of different MC phenotypes are still not well understood. MCs are present in blood vessel walls, but their specific [...] Read more.
Mast cells (MCs) are distributed in tissues throughout the body and are highly involved in many physiological and pathophysiological processes. The potential and involvement of different MC phenotypes are still not well understood. MCs are present in blood vessel walls, but their specific phenotypic features are unknown. We aimed at characterizing MCs from human saphenous veins for localization, mediator content, and receptor expression. This was done in MCs from both healthy and varicose human saphenous veins (hSV and vSV, respectively). For both vSV and hSV, we found that vein MCs are mainly present in the tunica adventitia (99% MCs in adventitia) and that the population consists of both MCT and MCTC phenotypes (vSV: 55% MCT, hSV: 64% MCT). The vein MCs contained high levels of histamine (vSV: 27 pg/MC, hSV: 55 pg/MC) and tryptase (vSV: 98 pg/MC, hSV: 111 pg/MC), indicating a strong potential for regulatory effects on blood vessels. The receptor expression of FcεRI, MRGPRX2, PTAFR, C3aR, and C5aR was found, even though the percentage of positive cells differed between vSV and hSV MCs. We conclude that vein MCs from the blood vessel wall have a high potential to affect the tissue around them. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Anaphylaxis)
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