Allergic Response

2019 ◽  
Author(s):  
Joud Hajjar ◽  
Lawrence B Schwartz
Keyword(s):  
Mast Cell ◽  
Immunoglobulin E ◽  
Signs And Symptoms ◽  
Specific Ige ◽  
Consensus Conference ◽  
Allergic Response ◽  
Working Definition ◽  
Keywords Allergy ◽  
Ige Mediated ◽  
Definition Of

The term hypersensitivity refers to diseases caused by an immune response, regardless of whether the response is against a pathogen, nonpathogen, or self and regardless of whether the response is directed by antibodies, lymphocytes, or innate pathways. The term anaphylaxis was coined in 1902 by Charles Richet, who received the Nobel Prize in 1913; this systemic allergic response is now known to be an immediate hypersensitivity reaction, initiated by allergen delivered to a host having allergen-specific IgE, thereby causing an IgE-mediated immunologic response and activating mast cells and basophils to secrete bioactive mediators. In 2005, the National Institutes of Health organized a consensus conference to develop a working definition of anaphylaxis, designed to be used by physicians at the bedside, as a serious allergic reaction that is rapid in onset, typically eliciting various combinations of cutaneous, cardiovascular, respiratory, and gastrointestinal manifestations, and may cause death.1,2 This facilitated the early treatment of such patients with epinephrine. Confusion arises over the misapplication of the term allergy or hypersensitivity to describe any untoward reaction to food, medications, or environmental exposures. Furthermore, non–IgE-mediated forms of local and systemic mast cell or basophil activation events can occur, causing signs and symptoms similar to those mediated by IgE.  This review contains 3 figures, 9 tables, and 62 references. Keywords: allergy, hypersensitivity, anaphylaxis, interleukin, chemokines, immunoglobulin E, mast cell, eosinophil

Allergic Response

2019 ◽  
Author(s):  
Joud Hajjar ◽  
Lawrence B Schwartz
Keyword(s):  
Mast Cell ◽  
Immunoglobulin E ◽  
Signs And Symptoms ◽  
Specific Ige ◽  
Consensus Conference ◽  
Allergic Response ◽  
Working Definition ◽  
Keywords Allergy ◽  
Ige Mediated ◽  
Definition Of

The term hypersensitivity refers to diseases caused by an immune response, regardless of whether the response is against a pathogen, nonpathogen, or self and regardless of whether the response is directed by antibodies, lymphocytes, or innate pathways. The term anaphylaxis was coined in 1902 by Charles Richet, who received the Nobel Prize in 1913; this systemic allergic response is now known to be an immediate hypersensitivity reaction, initiated by allergen delivered to a host having allergen-specific IgE, thereby causing an IgE-mediated immunologic response and activating mast cells and basophils to secrete bioactive mediators. In 2005, the National Institutes of Health organized a consensus conference to develop a working definition of anaphylaxis, designed to be used by physicians at the bedside, as a serious allergic reaction that is rapid in onset, typically eliciting various combinations of cutaneous, cardiovascular, respiratory, and gastrointestinal manifestations, and may cause death.1,2 This facilitated the early treatment of such patients with epinephrine. Confusion arises over the misapplication of the term allergy or hypersensitivity to describe any untoward reaction to food, medications, or environmental exposures. Furthermore, non–IgE-mediated forms of local and systemic mast cell or basophil activation events can occur, causing signs and symptoms similar to those mediated by IgE.  This review contains 3 figures, 9 tables, and 62 references. Keywords: allergy, hypersensitivity, anaphylaxis, interleukin, chemokines, immunoglobulin E, mast cell, eosinophil

scholarly journals The transcriptional program, functional heterogeneity, and clinical targeting of mast cells

2017 ◽  
Vol 214 (9) ◽  
pp. 2491-2506 ◽  
Author(s):  
Gökhan Cildir ◽  
Harshita Pant ◽  
Angel F. Lopez ◽  
Vinay Tergaonkar
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Immunoglobulin E ◽  
Inflammatory Diseases ◽  
Small Population ◽  
Transcriptional Program ◽  
Cell Functions ◽  
New Concepts ◽  
Health And Disease ◽  
Ige Mediated

Mast cells are unique tissue-resident immune cells that express an array of receptors that can be activated by several extracellular cues, including antigen–immunoglobulin E (IgE) complexes, bacteria, viruses, cytokines, hormones, peptides, and drugs. Mast cells constitute a small population in tissues, but their extraordinary ability to respond rapidly by releasing granule-stored and newly made mediators underpins their importance in health and disease. In this review, we document the biology of mast cells and introduce new concepts and opinions regarding their role in human diseases beyond IgE-mediated allergic responses and antiparasitic functions. We bring to light recent discoveries and developments in mast cell research, including regulation of mast cell functions, differentiation, survival, and novel mouse models. Finally, we highlight the current and future opportunities for therapeutic intervention of mast cell functions in inflammatory diseases.

Aqueous Extract of Mosla chinensis Inhibits Mast Cell-Mediated Allergic Inflammation

2012 ◽  
Vol 40 (06) ◽  
pp. 1257-1270 ◽  
Author(s):  
Hui-Hun Kim ◽  
Jin-Su Yoo ◽  
Tae-Yong Shin ◽  
Sang-Hyun Kim
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Histamine Release ◽  
Aqueous Extract ◽  
Proinflammatory Cytokines ◽  
Immunoglobulin E ◽  
Inflammatory Diseases ◽  
Allergic Inflammation ◽  
Inhibitory Effect ◽  
Ige Mediated

Allergic inflammatory diseases such as food allergy, asthma, sinusitis, and atopic dermatitis are increasing worldwide. In this study, we investigated the effects of aqueous extract of Mosla chinensis Max. (AMC) on mast cell-mediated allergic inflammation and studied the possible mechanism of this action. AMC inhibited compound 48/80-induced systemic and immunoglobulin E (IgE)-mediated local anaphylaxis. AMC reduced intracellular calcium levels and downstream histamine release from rat peritoneal mast cells activated by compound 48/80 or IgE. In addition, AMC decreased gene expression and secretion of proinflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-8 in human mast cells. The inhibitory effect of AMC on cytokine expression was nuclear factor (NF)-κB dependent. Our results indicate that AMC inhibits mast cell-mediated allergic inflammatory reaction by suppressing histamine release and expression of proinflammatory cytokines and the involvement of calcium and NF-κB in these effects. AMC might be a possible therapeutic candidate for allergic inflammatory disorders.

scholarly journals Denatonium Benzoate Exposure Promotes IgE-Mediated Mast Cell Degranulation and Allergy By Upregulating FcεRIα Expression

2021 ◽  
Author(s):  
Huaping Xu ◽  
Xiaoyun Shi ◽  
Mengting Xie ◽  
Shiyu Xiao ◽  
Xin Li ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Cell Surface ◽  
Surface Expression ◽  
Specific Ige ◽  
Mast Cell Degranulation ◽  
Cell Surface Expression ◽  
Denatonium Benzoate ◽  
Ige Mediated

Abstract Background: Denatonium benzoate (DB), one of the bitterest compounds known to man, is currently added to a wide range of products and is also used for alcohol denaturation. Some reports demonstrated that asthmatic symptoms are associated with DB exposure but the possible links between DB and IgE-mediated allergy susceptibility have not been examined to date. We investigated the effects of DB on IgE-mediated mast cell degranulation in vitro and in the ovalbumin (OVA)-induced mouse model of allergy.Methods: DB treatments were given to RBL-2H3 IgE-sensitized rat mast cell/basophil cells and KU812 human basophilic cells together with OVA-induced allergic BALB/c mice. Allergic mediator release, Ca2+ influx and OVA-specific IgE anaphylactic shock symptoms were measured along with the cell-surface expression of the α-subunit of high-affinity IgE receptor FcεRI on mast cells.Results: DB increases β-hexosaminidase (β-hex) release and Ca2+ mobilization in IgE-mediated activated RBL-2H3 and KU812 cells, and enhanced the cell-surface expression of FcεRIα. DB also promoted the severity of OVA-induced anaphylactic and diarrheic symptoms which was accompanied by mucus thickness in jejunum and the levels of β-hex, histamine and OVA-specific IgE in allergy mice, as well as the levels of FcεRIα mRNA and the FcεRIα proteinin isolated mucosal mast cells. Conclusions: DB treatments can promote the IgE-mediated mast cell degranulation in vitro and OVA-induced allergic susceptibility in mice by upregulating mast-cell-surface FcεR1α expression, providing evidence for DB exposure in promoting allergy susceptibility.

scholarly journals Evolutionary background of allergic reactivity: mast cells, FcεRI, IgE - three components of the effector phase of the allergic response

2018 ◽  
Vol 15 (4) ◽  
pp. 5-16
Author(s):  
I S Gushchin
Keyword(s):  
Mast Cells ◽  
Immunoglobulin E ◽  
The Body ◽  
Allergic Response ◽  
Effector Phase ◽  
Time Regime ◽  
High Affinity Receptor ◽  
Ige Mediated ◽  
Affinity Receptor ◽  
Elimination Function

The literature data on the evolution of the main obligatory participants in the effector phase of the IgE-mediated allergic response are presented: mast cells/basophils, immunoglobulin E, and high affinity receptor for the Fcε fragment (FcεRI). Allergic reactivity is considered as the most recent evolutionary immunologically-mediated acquisition of mammals. It is aimed at recognizing small amounts of allergen entering the body in a certain time regime, and organizing an allergen-specific inflammation that carries features of elimination function. The most biologically justified way to prevent allergies is to restore the function of barrier systems and, accordingly, to prevent the need to develop an allergic response.

scholarly journals Decreased Histone Acetylation Levels at Th1 and Regulatory Loci after Induction of Food Allergy

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3193
Author(s):  
Bilal Alashkar Alhamwe ◽  
Laura A. P. M. Meulenbroek ◽  
Désirée H. Veening-Griffioen ◽  
Tjalling M. D. Wehkamp ◽  
Fahd Alhamdan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Food Allergy ◽  
Histone Acetylation ◽  
Specific Ige ◽  
Allergic Response ◽  
Cow’S Milk ◽  
Milk Allergy ◽  
T Helper ◽  
Cow's Milk ◽  
Ige Mediated

Immunoglobulin E (IgE)-mediated allergy against cow’s milk protein fractions such as whey is one of the most common food-related allergic disorders of early childhood. Histone acetylation is an important epigenetic mechanism, shown to be involved in the pathogenesis of allergies. However, its role in food allergy remains unknown. IgE-mediated cow’s milk allergy was successfully induced in a mouse model, as demonstrated by acute allergic symptoms, whey-specific IgE in serum, and the activation of mast cells upon a challenge with whey protein. The elicited allergic response coincided with reduced percentages of regulatory T (Treg) and T helper 17 (Th17) cells, matching decreased levels of H3 and/or H4 histone acetylation at pivotal Treg and Th17 loci, an epigenetic status favoring lower gene expression. In addition, histone acetylation levels at the crucial T helper 1 (Th1) loci were decreased, most probably preceding the expected reduction in Th1 cells after inducing an allergic response. No changes were observed for T helper 2 cells. However, increased histone acetylation levels, promoting gene expression, were observed at the signal transducer and activator of transcription 6 (Stat6) gene, a proallergic B cell locus, which was in line with the presence of whey-specific IgE. In conclusion, the observed histone acetylation changes are pathobiologically in line with the successful induction of cow’s milk allergy, to which they might have also contributed mechanistically.

scholarly journals Additives and preservatives: Role in food allergy

2020 ◽  
Vol 2 (1) ◽  
pp. 119-123
Author(s):  
Amber N. Pepper ◽  
Panida Sriaroon ◽  
Mark C. Glaum
Keyword(s):  
Food Allergy ◽  
Immunoglobulin E ◽  
Skin Prick Testing ◽  
Food Additives ◽  
Specific Ige ◽  
Food Additive ◽  
Blood Testing ◽  
Commercial Products ◽  
Natural Substances ◽  
Ige Mediated

Food additives are natural or synthetic substances added to foods at any stage of production to enhance flavor, texture, appearance, preservation, safety, or other qualities. Common categories include preservatives and antimicrobials, colorings and dyes, flavorings, antioxidants, stabilizers, and emulsifiers. Natural substances rather than synthetics are more likely to cause hypersensitivity. Although rare, food additive hypersensitivity should be suspected in patients with immunoglobulin E (IgE)-mediated reactions to multiple, unrelated foods, especially if the foods are prepared outside of the home or when using commercial products. A complete and thorough history is vital. Skin prick testing and/or specific IgE blood testing to food additives, if available, additive avoidance diets, and blind oral challenges can help establish the diagnosis. Once an allergy to a food additive is confirmed, management involves avoidance and, if necessary, carrying self-injectable epinephrine.

scholarly journals Immunoglobulin E as a biomarker for the overlap of atopic asthma and chronic obstructive pulmonary disease

2019 ◽  
Author(s):  
Craig P. Hersh ◽  
Soumya Zacharia ◽  
Ram Prakash Arivu Chelvan ◽  
Lystra P. Hayden ◽  
Ali Mirtar ◽  
...  
Keyword(s):  
Immunoglobulin E ◽  
Specific Ige ◽  
Clinical Syndrome ◽  
Chest Ct ◽  
Self Report ◽  
Atopic Asthma ◽  
Wall Thickening ◽  
Chronic Obstructive ◽  
Total Ige ◽  
Definition Of

AbstractAsthma-COPD overlap (ACO) is a common clinical syndrome, yet there is no single objective definition. We hypothesized that Immunoglobulin E measurements could be used to refine the definition of ACO. In baseline plasma samples from 2870 subjects in the COPDGene Study, we measured total IgE levels and specific IgE levels to six common allergens. Compared to usual COPD, subjects with ACO had higher total IgE levels (median 67.0 vs 42.2 IU/ml) and more frequently had at least one positive specific IgE (43.5 vs 24.5%). We previously used a strict definition of ACO in subjects with COPD, based on self-report of a doctor’s diagnosis of asthma before the age of 40. This strict ACO definition was refined by the presence of atopy, determined by total IgE >100 IU/ml or at least one positive specific IgE, as was a broader definition of ACO based on any asthma history. Subjects will all three ACO definitions were younger (mean age 60.0-61.3), were more commonly African American (36.8-44.2%), had a higher exacerbation frequency (1.0-1.2 in the past year), and had more airway wall thickening on quantitative analysis of chest CT scans. Among subjects with clinical ACO, 37-46% did not have atopy; these subjects had more emphysema on chest CT scan. Based on associations with exacerbations and CT airway disease, IgE did not clearly improve the clinical definition of ACO. However, IgE measurements could be used to subdivide subjects with atopic and non-atopic ACO, who might have different biologic mechanisms and potential treatments.

Intestinal anaphylaxis: in vivo and in vitro studies of the rat proximal colon

1988 ◽  
Vol 255 (2) ◽  
pp. G201-G205 ◽  
Author(s):  
D. Forbes ◽  
M. Patrick ◽  
M. Perdue ◽  
A. Buret ◽  
D. G. Gall
Keyword(s):  
Mast Cell ◽  
Immunoglobulin E ◽  
Short Circuit ◽  
Proximal Colon ◽  
Antigen Challenge ◽  
Food Protein ◽  
Ussing Chambers ◽  
Cl Secretion ◽  
Ige Mediated

The response of the rat proximal colon to an immunoglobulin E (IgE)-mediated hypersensitivity reaction was examined. Rats were sensitized to egg albumin (EA) by intraperitoneal injection, and serum titers of specific anti-EA IgE were measured at 14 days. Sensitized animals had titers of greater than or equal to 1:64, whereas no anti-EA IgE antibodies were detected in controls. Water and electrolyte absorption in the proximal colon, before and during antigen challenge, was measured by in vivo marker perfusion. Antigen challenge resulted in significant inhibition of water, Na+, Cl-, and K+ absorption in vivo. Proximal colonic tissue from sensitized and control animals was studied in Ussing chambers under short-circuited conditions. Antigen challenge of sensitized tissue resulted in significant increases in short-circuit current due to the induction of active Cl- secretion. No such changes were seen in control tissue. The abnormalities induced by antigen challenge in tissue from sensitized animals was blocked by doxantrazole (10(-3) M), a mast cell stabilizer. The findings indicate that IgE-mediated reactions in rat proximal colon to a food protein cause pertubations in water and electrolyte transport secondary to active Cl- secretion and these abnormalities appear to be due to mast cell degranulation.

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