Anaphylaxis

2019 ◽  
Author(s):  
Cem Akin

Anaphylaxis, a serious allergic reaction, is rapid in onset and marked by flushing, urticaria, angioedema, pruritus, bronchospasm, and abdominal cramping with nausea, vomiting, and diarrhea. It is not uncommon; approximate lifetime prevalence of anaphylaxis was estimated to be 0.5 to 2% or possibly higher due to the common academic belief that the incidence of anaphylactic reactions is underreported. Rarely, anaphylaxis may cause death, most commonly from drugs, foods, and insect stings. This review covers the epidemiology, etiology, pathogenesis, diagnosis, clinical manifestations, treatment, and prognosis. Figures show inflammatory pathways in allergic inflammation and mast cell degranulation and pathways of activation.  This review contains 2 figures, 5 tables, and 72 references.  Keywords: Anaphylaxis, allergy, shock, auto-injector epinephrine, inflammation, mast cell, venom

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Douglas B. Aidoo ◽  
David D. Obiri ◽  
Newman Osafo ◽  
Aaron O. Antwi ◽  
Leslie B. Essel ◽  
...  

Bergapten (5-methoxypsoralen, 5-MOP) is a plant-derived furocoumarin with demonstrated anti-inflammatory action. The present study investigated its effects on allergic inflammation in two related pathways of mast cell degranulation. Compound 48/80 and lipopolysaccharide (LPS) were used to activate the IgE-independent pathway while bovine serum albumin (BSA) was used as allergen for the IgE-dependent pathway. The modulatory effect of bergapten on mast cell degranulation, neutrophil extravasation, protein concentration, lung histopathology, and oxidative stress was assessed. Bergapten at 10, 30, and 100 μg/ml for 15 min stabilized mast cells in rat mesenteric tissue from disruption in vitro and when administered in vivo at 3, 10, and 30 mg kg−1 for 1 h protected mice from fatal anaphylaxis induced by compound 48/80. Similarly, treatment of LPS-challenged mice with bergapten (3, 10, and 30 mg kg−1) for 24 h significantly decreased neutrophil infiltration into bronchoalveolar lavage fluid, mean protein concentration, and inflammatory cell infiltration of pulmonary tissues when compared to the saline-treated LPS-challenged control. In addition, lung histology of the bergapten-treated LPS-challenged mice showed significantly less oedema, congestion, and alveolar septa thickening when compared to the saline-treated LPS-challenged disease control. LPS-induced oxidative stress was significantly reduced through increased tissue activities of catalase and superoxide dismutase and reduced malondialdehyde levels on treatment with bergapten. In the triple antigen-induced active anaphylaxis, daily administration of bergapten at 3, 10, and 30 mg kg−1 for 10 days, respectively, protected previously sensitized and challenged mice against anaphylactic shock. Overall, our study demonstrates the ability of bergapten to attenuate allergic airway-induced hypersensitivity in murine models of inflammation, suggesting its possible therapeutic benefit in this condition.


2005 ◽  
Vol 289 (5) ◽  
pp. L856-L866 ◽  
Author(s):  
Delphine C. Malherbe ◽  
Veit J. Erpenbeck ◽  
Soman N. Abraham ◽  
Erika C. Crouch ◽  
Jens M. Hohlfeld ◽  
...  

Mast cells play a key role in allergy and asthma. They reside at the host-environment interface and are among the first cells to make contact with inhaled microorganisms and particulate antigens. Pulmonary surfactant proteins A and D (SP-A and SP-D) function in lung host defense by enhancing microbe phagocytosis and mediating other immune cell functions, but little is known about their effects on mast cells. We hypothesized that SP-A and/or SP-D modulate IgE-dependent mast cell functions. Pollen starch granules (PSG) extracted from Dactylis glomerata and coated with trinitrophenol (TNP) were used as a model of an inhaled organic particulate allergen. Our data revealed that SP-D inhibited by 50% the release of β-hexosaminidase by peritoneal mast cells sensitized with IgE anti-TNP and stimulated with TNP-PSG. In contrast, SP-A had no effect. Furthermore, SP-D aggregated PSG in a dose-dependent manner, and this aggregation was mediated by SP-D's carbohydrate recognition domain. A single arm SP-D mutant (RrSP-Dser15,20) neither aggregated PSG nor inhibited degranulation, suggesting that multimerization of SP-D is required for maximal PSG aggregation and inhibition of PSG-induced mast cell degranulation. This study is the first to demonstrate that SP-D modulates IgE-mediated mast cell functions, which are important in asthma and allergic inflammation.


2007 ◽  
Vol 21 (6) ◽  
pp. 783-790 ◽  
Author(s):  
Frederico Azevedo Costa-Pinto ◽  
Alexandre Salgado Basso ◽  
Momtchilo Russo

2013 ◽  
Vol 18 (10) ◽  
pp. 1223-1233 ◽  
Author(s):  
Rejbinder Kaur ◽  
Lisa A. Sloan ◽  
Andy D. Blanchard ◽  
Janet L. Smith ◽  
Ian Churcher ◽  
...  

Mast cells are unique hematopoietic cells that are richly distributed in the skin and mucosal surfaces of the respiratory and gastrointestinal tract. They play a key role in allergic inflammation by releasing a cocktail of granular constituents, including histamine, serine proteases, and various eicosanoids and cytokines. As such, a number of drugs target either inhibition of mast cell degranulation or the products of degranulation. To identify potential novel drugs and mechanisms in mast cell biology, assays were developed to identify inhibitors of mast cell degranulation and activation in a phenotypic screen. Due to the challenges associated with obtaining primary mast cells, cord blood–derived mononuclear cells were reproducibly differentiated to mast cells and assays developed to monitor tryptase release and prostaglandin D2 generation. The tryptase assay was particularly sensitive, requiring only 500 cells per data point, which permitted a set of approximately 12,000 compounds to be screened robustly and cost-effectively. Active compounds were tested for concomitant inhibition of prostaglandin D2 generation. This study demonstrates the robustness and effectiveness of this approach in the identification of potential novel compounds and mechanisms targeting mast cell–driven inflammation, to enable innovative drug discovery efforts to be prosecuted.


Allergy ◽  
2019 ◽  
Vol 75 (5) ◽  
pp. 1155-1164 ◽  
Author(s):  
Inge Kortekaas Krohn ◽  
Sven F. Seys ◽  
Gitte Lund ◽  
Anne‐Charlotte Jonckheere ◽  
Isabelle Dierckx de Casterlé ◽  
...  

1971 ◽  
Vol 33 (3) ◽  
pp. 223-228
Author(s):  
Shojiro MORIYASU

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yapeng Li ◽  
Junfeng Gao ◽  
Mohammad Kamran ◽  
Laura Harmacek ◽  
Thomas Danhorn ◽  
...  

AbstractMast cells are critical effectors of allergic inflammation and protection against parasitic infections. We previously demonstrated that transcription factors GATA2 and MITF are the mast cell lineage-determining factors. However, it is unclear whether these lineage-determining factors regulate chromatin accessibility at mast cell enhancer regions. In this study, we demonstrate that GATA2 promotes chromatin accessibility at the super-enhancers of mast cell identity genes and primes both typical and super-enhancers at genes that respond to antigenic stimulation. We find that the number and densities of GATA2- but not MITF-bound sites at the super-enhancers are several folds higher than that at the typical enhancers. Our studies reveal that GATA2 promotes robust gene transcription to maintain mast cell identity and respond to antigenic stimulation by binding to super-enhancer regions with dense GATA2 binding sites available at key mast cell genes.


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