Mast Cells in Allergic and Inflammatory Diseases

Sismanopoulos, Nikolaos; Delivanis, Danae-Anastasia; Alysandratos, Konstantinos-Dionysios; Angelidou, Asimenia; Therianou, Anastasia; Kalogeromitros, Dimitrios; C. Theoharides, Theoharis

doi:10.2174/138161212800165997

Cited by 87Mast cells and histamineAsthma and respiratory diseasesFood Allergy and Anaphylaxis Research

Mast Cells in Allergic and Inflammatory Diseases

Sismanopoulos, Nikolaos, Delivanis, Danae-Anastasia, Alysandratos, Konstantinos-Dionysios, Angelidou, Asimenia, Therianou, Anastasia, Kalogeromitros, Dimitrios, C. Theoharides, Theoharis·2012·Current Pharmaceutical Design

DOI 10.2174/138161212800165997

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Abstract

Mast cells are important in the development of allergic and anaphylactic reactions, but also in acquired and innate immunity. There is also increasing evidence that mast cells participate in inflammatory diseases, where they can be activated by non-allergic triggers, such as neuropeptides and cytokines, often having synergistic effects as in the case of substance P (SP) and IL-33. Secretion of vasoactive mediators, cytokines and proteinases contribute to the development of coronary artery disease (CAD), as well as to diet-induced obesity and the metabolic syndrome. Mast cells may be able to orchestrate such different biological processes through their ability to release pro-inflammatory mediators selectively without the degranulation typical of allergic reactions. Recent evidence suggests that mitochondrial uncoupling protein 2 (UCP2) and mitochondrial translocation regulate mast cell degranulation, but not selective mediator release. Better understanding of these two processes and how mast cells exert both immunostimulatory and immunosuppressive actions could lead to the development of inhibitors of release of specific mediators with novel therapeutic applications.

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Gut-Microbiota-Brain Axis and Its Effect on Neuropsychiatric Disorders With Suspected Immune Dysregulation
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“MCs can be activated by a variety of stimulating factors, including IgE-specific antigens, complement components, neuropeptides such as somatostatin and substance P, cytokines, microbial products, and physical stimuli [9].”
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IL-33 induces IL-13 production by mouse mast cells independently of IgE-FcεRI signals
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Authors: Sismanopoulos, N., Delivanis, D.-A., Alysandratos, K.-D., Angelidou, A., Therianou, A., Kalogeromitros, D., & C. Theoharides, T.
Affiliations: Tufts University (US)
ORCID: Alysandratos, Konstantinos-Dionysios
Angelidou, Asimenia
Venue: Current Pharmaceutical Design
Publisher: Bentham Science Publishers Ltd.
Published: 2012-04-01
Volume: 18
Issue: 16
Pages: 2261-2277
ISSN: 1381-6128 (ISSN-L)
DOI: 10.2174/138161212800165997
OpenAlex: W2151711434
Cited by: 87
References: 349
Citations by year: 2026: 3 · 2025: 3 · 2024: 3 · 2023: 4 · 2022: 3 · 2021: 6 · 2020: 8 · 2019: 5 · 2018: 8 · 2017: 7 · 2016: 7 · 2015: 15 · 2014: 8 · 2013: 7
FWCI: 4.18
Type: journal article
Language: en
Open access: closed
Locations: Current Pharmaceutical Design (publishedVersion)
PubMed (publishedVersion)
Funders: State Scholarships Foundation
National Institutes of Health (5r01ns066205-05)
National Institute of Neurological Disorders and Stroke (NS55681, NS71361, R01NS071361, NS 66205)
National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR 47652, R01AR047652)
Topics: Life Sciences › Immunology and Microbiology › Immunology › Mast cells and histamine
Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
Health Sciences › Medicine › Immunology and Allergy › Food Allergy and Anaphylaxis Research
Keywords: mast cells, allergic reactions, anaphylaxis, inflammatory diseases, substance P, IL-33, neuropeptides, cytokines, coronary artery disease, diet-induced obesity, metabolic syndrome, mast cell degranulation, UCP2, mitochondrial uncoupling, immunosuppression
MeSH terms: Coronary Artery Disease, Diabetes Mellitus, Humans, Hypersensitivity, Inflammation, Mast Cells, Inflammation Mediators

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Mast Cells in Allergic and Inflammatory Diseases

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