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Journal articles on the topic 'Allergic response'
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1
Martin, Lynn B., and Courtney A. C. Coon. "Photoperiod-driven variation in an allergic response is independent of allergen exposure." Canadian Journal of Zoology 90, no. 9 (September 2012): 1086–93. http://dx.doi.org/10.1139/z2012-075.
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Allergy prevalence and severity varies seasonally in humans, presumably due to intra-annual changes in allergen exposure. However, it is possible that seasonality of allergic responses is also influenced by seasonal changes in the immune system. Here, we asked whether extended exposure to different day lengths would alter allergic responses to pentadecylcatechol (PDC), an allergenic component of poison ivy ( Toxicodendron radicans (L.) Kuntze), in Siberian hamsters ( Phodopus sungorus (Pallas, 1773)), a species exhibiting extensive seasonal variation in immune functions. We found that contact dermatitis responses were larger in short day-length (SD) housed animals than in long day-length (LD) housed animals even though sensitization and challenge dosages of allergen were identical. Furthermore, SD animals were smaller and had regressed reproductive tissues compared with LD animals, results typically observed in this species in response to photoperiod. These data suggest that endogenous changes in immune functions, perhaps via melatonin, may underlie some seasonal variation in allergic responses.
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Roger, Albert, Maria Basagana, Aina Teniente-Serra, Nathalie Depreux, Yanina Jurgens, Clara Padro, Sira Miquel, Carolina Elduque, and Eva M. Martinez-Caceres. "Immunotheraphy in Allergic Diseases." Current Pharmaceutical Design 24, no. 11 (June 27, 2018): 1174–94. http://dx.doi.org/10.2174/1381612824666180116094048.
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The prevalence of allergic diseases is increasing worldwide. It is estimated that more than 30% of the world population is now affected by one or more allergic conditions and a high proportion of this increase is in young people. The diagnosis of allergy is dependent on a history of symptoms on exposure to an allergen together with the detection of allergen-specific IgE. Accurate diagnosis of allergies opens up therapeutic options. Allergen specific immunotherapy is the only successful disease-modifying therapy for IgE-mediated allergic diseases. New therapeutic strategies have been developed or are currently under clinical trials. Besides new routes of administration, new types of allergens are being developed. The use of adjuvants may amplify the immune response towards tolerance to the antigens. In this review, we analyze different antigen-specific immunotherapies according to administration route, type of antigens and adjuvants, and we address the special case of food allergy.
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Besedovsky, Luciana, Mona Benischke, Jörg Fischer, Amir S. Yazdi, and Jan Born. "Human sleep consolidates allergic responses conditioned to the environmental context of an allergen exposure." Proceedings of the National Academy of Sciences 117, no. 20 (May 4, 2020): 10983–88. http://dx.doi.org/10.1073/pnas.1920564117.
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Allergies are highly prevalent, and allergic responses can be triggered even in the absence of allergens due to Pavlovian conditioning to a specific cue. Here we show in humans suffering from allergic rhinitis that merely reencountering the environmental context in which an allergen was administered a week earlier is sufficient to trigger an allergic response—but only if participants had slept after allergen exposure. This context-conditioning effect was entirely absent when participants stayed awake the night after allergen exposure or were tested in a different context. Unlike in context conditioning, cue conditioning (to an odor stimulus) occurred independently of sleep, a differential pattern that is likewise observed for conditioning in the behavioral domain. Our findings provide evidence that allergic responses can be conditioned to contextual information alone, even after only a single-trial conditioning procedure, and that sleep is necessary to consolidate this rapidly acquired maladaptive response. The results unravel a mechanism that could explain part of the strong psychological impact on allergic responses.
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Jacquet, Alain. "Innate Immune Responses in House Dust Mite Allergy." ISRN Allergy 2013 (February 28, 2013): 1–18. http://dx.doi.org/10.1155/2013/735031.
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Sensitizations to house dust mites (HDM) trigger strong exacerbated allergen-induced inflammation of the skin and airways mucosa from atopic subjects resulting in atopic dermatitis as well as allergic rhinitis and asthma. Initially, the Th2-biased HDM allergic response was considered to be mediated only by allergen B- and T-cell epitopes to promote allergen-specific IgE production as well as IL-4, IL-5, and IL-13 to recruit inflammatory cells. But this general molecular model of HDM allergenicity must be revisited as a growing literature suggests that stimulations of innate immune activation pathways by HDM allergens offer new answers to the following question: what makes an HDM allergen an allergen? Indeed, HDM is a carrier not only for allergenic proteins but also microbial adjuvant compounds, both of which are able to stimulate innate signaling pathways leading to allergy. This paper will describe the multiple ways used by HDM allergens together with microbial compounds to control the initiation of the allergic response through engagement of innate immunity.
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Dr. Mayank Surana, Dr. Vineeta Pande, Dr. Sharad Agarkhedkar, and Dr. Ajit Teegala. "Correlation between Total Serum Immunoglobulin E (IgE) and Absolute Eosinophil Count (AEC) in Allergic Diseases In Children." VIMS Health Science Journal 7, no. 1 (March 6, 2020): 5–9. http://dx.doi.org/10.46858/vimshsj.7102.
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Allergy, is a clinical expression of soluble factors like IgE, histamine or eosinophils found in serum or plasma of such patients. The products that are responsible for allergy are called as Allergens. Allergens normally induce IgE production which leads to type 1 hypersensitivity response on subsequent exposure to the same allergen. The target organs are mostly nose, lung, skin and gastrointestinal tract. Atopy is also considered as a triad of Atopic dermatitis, allergic rhinitis and bronchial asthma. Raised serum IgE and AEC are proven indicators of allergic phenomenon. Various studies show relationship between serum Immunoglobulin E level and total eosinophil count in population suffering from allergic diseases. Serum total Immunoglobulin E, total eosinophil count and specific IgE are all helpful for the diagnosis and treatment of allergic diseases. Objectives: 1.To Evaluate Serum Total IgE level in Children with allergic diseases.2. To Evaluate Absolute Eosinophil Count (AEC) in children with allergic diseases.3. To Correlate Serum Total Immunoglobulin E Level and Absolute Eosinophil Count (AEC) with allergic diseases. Methodology: Cross sectional study with 100 children in the age group 2-12 years with nasopharyngeal allergies (like bronchial asthma and atopic rhinitis) and skin allergies (like atopic dermatitis, urticaria) ,eye allergies were enrolled and serum IgE levels and AEC levels was done. Results: In present study Absolute eosinophil count was raised in 58% of cases Serum IgE was raised in 54% of cases. In present study, of 58% cases with raised Absolute eosinophil count 81% (47 cases) showed raised serum IgE levels. Conclusion: Absolute eosinophil count and serum Total IgE has been considered as a significant marker of allergic state and can be used as a marker of allergic response in atopic individuals. Raised serum IgE and AEC are more in nasobronchial allergy as compare to other systemic allergies. The elevated level of serum Total IgE and Absolute Eosinophil Count both shows Significant Correlation thus can be considered as a dependable laboratory investigation in diagnosing and categorizing allergic diseases.
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Deak, Peter E., Baksun Kim, Amina Abdul Qayum, Jaeho Shin, Girish Vitalpur, Kirsten M. Kloepfer, Matthew J. Turner, et al. "Designer covalent heterobivalent inhibitors prevent IgE-dependent responses to peanut allergen." Proceedings of the National Academy of Sciences 116, no. 18 (April 8, 2019): 8966–74. http://dx.doi.org/10.1073/pnas.1820417116.
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Allergies are a result of allergen proteins cross-linking allergen-specific IgE (sIgE) on the surface of mast cells and basophils. The diversity and complexity of allergen epitopes, and high-affinity of the sIgE–allergen interaction have impaired the development of allergen-specific inhibitors of allergic responses. This study presents a design of food allergen-specific sIgE inhibitors named covalent heterobivalent inhibitors (cHBIs) that selectively form covalent bonds to only sIgEs, thereby permanently inhibiting them. Using screening reagents termed nanoallergens, we identified two immunodominant epitopes in peanuts that were common in a population of 16 allergic patients. Two cHBIs designed to inhibit only these two epitopes completely abrogated the allergic response in 14 of the 16 patients in an in vitro assay and inhibited basophil activation in an allergic patient ex vivo analysis. The efficacy of the cHBI design has valuable clinical implications for many allergen-specific responses and more broadly for any antibody-based disease.
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Simbirtsev, A. S. "Cytokines and their role in immune pathogenesis of allergy." Russian Medical Inquiry 5, no. 1 (2021): 32–37. http://dx.doi.org/10.32364/2587-6821-2021-5-1-32-37.
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Allergy is characterized by inadequate hyperimmune response to one or several antigens with the properties of allergens. A specific pattern of abnormal synthesis of some cytokines (principal molecular mediators of the initiation, development, and regulation of allergic inflammation) has an important pathogenic role in allergy. In recent years, it is generally accepted that allergic disorders are accounted for by impaired immune regulation resulting from increased imbalanced activation of allergen-specific T helper 2 cell clones. Allergic type of immune response is currently referred to as type 2 immune response which normally provides humoral immunity, anthelmintic protection etc. However, pathological response results in allergy. Studies on immune pathogenesis of allergic disorders have improved our understanding of the role of altered synthesis of some cytokines (key mediators of allergic inflammation). Cytokines involved in the initiation and regulation of allergy are produced by epithelial cells, various subsets of leukocytes, innate lymphoid cells, and allergen-activated T helper cell clones. Analysis of the associations of the changes in immune reactivity and clinical manifestations has established pathogenic heterogeneity and identified asthma phenotypes and endotypes. These findings have provided a basis for more reasonable, successful, and personalized approach to biological anti-cytokine treatment for allergic disorders. KEYWORDS: allergy, cytokines, T helper cell clones, phenotype, asthma, anti-cytokine therapy. FOR CITATION: Simbirtsev A.S. Cytokines and their role in immune pathogenesis of allergy. Russian Medical Inquiry. 2021;5(1):32–37. DOI: 10.32364/2587-6821-2021-5-1-32-37.
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Williams, Jesse W., Melissa Y. Tjota, and Anne I. Sperling. "The Contribution of Allergen-Specific IgG to the Development of Th2-Mediated Airway Inflammation." Journal of Allergy 2012 (October 21, 2012): 1–9. http://dx.doi.org/10.1155/2012/236075.
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In both human asthmatics and animal models of allergy, allergen-specific IgG can contribute to Th2-mediated allergic inflammation. Mouse models have elucidated an important role for IgG and Fc-gamma receptor (FcγR) signaling on antigen presenting cells (APC) for the induction of airway inflammation. These studies suggest a positive feedback loop between IgG produced by the adaptive B cell response and FcγR signaling on innate immune cells. Studies of IgG and FcγRs in humans with asthma or allergic lung disease have been more controversial. Some reports have identified associations between allergen-specific IgG and severity of allergic responses, while other studies have found associations of IgG subclass IgG4 with allergic tolerance. In this paper, we review the literature to help define the nature of IgG and FcγR signaling on innate immune cells and how it contributes to the development of allergic immune responses.
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Lei, Dawn K., and Leslie C. Grammer. "An overview of allergens." Allergy and Asthma Proceedings 40, no. 6 (November 1, 2019): 362–65. http://dx.doi.org/10.2500/aap.2019.40.4247.
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Most allergens are proteins or glycoproteins that range in molecular weight from 5000 to 100,000 Da, although polysaccharides and low-molecular-weight substances may also be allergenic. Common allergens include pollens, fungal spores, house-dust mites, and animal epithelial materials but can also include drugs, biologic products, and insect venoms. The allergic response is dependent on the route of exposure. If the exposure is to an inhaled aeroallergen, then the allergic response will be respiratory in nature. Ingested or injected exposure gives rise to gastrointestinal, cutaneous, or anaphylactic reactions. The size of the pollen determines the clinical manifestation of allergy. For example, particles between 20 and 60 μm in diameter can be carried by the wind and cause nasal and ocular symptoms (allergic rhinoconjunctivitis). Particles of <7 μm can deposit in the airways and cause symptoms of asthma. Animals produce allergens in forms unique to each species. Cat allergen, most importantly Fel d 1, is buoyant and “sticky,” which means it easily remains airborne and may last in a home for up to 6 to 9 months after the source is removed. Cat allergen adheres to clothes and can be found in public places, e.g., schools. Dog allergen, particularly Can f 1, is present in dander, saliva, urine, and serum. All dog breeds produce allergenic proteins (even poodles and “hairless” dogs).
10
Gushchin, I. S. "Evolutionary background of allergic reactivity: mast cells, FcεRI, IgE - three components of the effector phase of the allergic response." Russian Journal of Allergy 15, no. 4 (December 15, 2018): 5–16. http://dx.doi.org/10.36691/rja131.
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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.
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Svirshchevskaya, E. V., M. A. Simonova, E. V. Matushevskaya, G. V. Fattakhova, S. V. Khlgatian, D. Yu Ryazantsev, D. B. Chudakov, and S. K. Zavriev. "Humoral response to Epstein-Barr viral infection in patients with allergies." Laboratory diagnostics, no. 1 (March 1, 2019): 57–64. http://dx.doi.org/10.24075/brsmu.2019.004.
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Type I hypersensitivity is mediated by the production of IgE antibodies in response to normally harmless substances. Debate still continues about the mechanisms underlying allergic reactions. Reduced barrier tissue function can be one of the risk factors for allergies. The aim of the present work was to compare the humoral immune response to Epstein-Barr virus in patients allergic to the A. alternata fungus or D. farinae house dust mites and healthy donors. It is known that up to 90% of the world population are infected with EBV. This infection occurs at early age when a child develops allergy. The antibodies were analyzed using immuno-PCR and the recombinant EBV protein rEBNA. We were able to demonstrate that infection occurs at early age in both allergic patients and healthy donors. The proportion of EBP-seropositive individuals was comparable between the groups (75% and 74%). The proportion of patients with high IgG1 titers among patients with allergies was lower (7%) than in healthy donors (18%), suggesting a lower viral load. In patients with allergies (but not in healthy donors) IgG1 titers declined as children grew older (р = 0.037). Besides, IgA1 titers were increased in patients with allergies in comparison with healthy donors, but differed between patients allergic to A. alternata and house dust mites. In allergic individuals, production of IgM against EBV was triggered earlier than in healthy donors. We conclude that IgM production and the IgA1-mediated humoral response occur earlier in patients with allergies, causing a decline in IgG1 titers over time.
12
Singh, Pramila, Mary Daniels, Darrell W. Winsett, Judy Richards, Donald Doerfler, Gary Hatch, Kenneth B. Adler, and M. Ian Gilmour. "Phenotypic comparison of allergic airway responses to house dust mite in three rat strains." American Journal of Physiology-Lung Cellular and Molecular Physiology 284, no. 4 (April 1, 2003): L588—L598. http://dx.doi.org/10.1152/ajplung.00287.2002.
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Brown Norway (BN) rats develop a robust response to antigens in the lung, characterized by a large increase in allergen-specific immune function and pulmonary eosinophilia. The objective of this study was to investigate alternative models by determining whether other rat strains could be sensitized to house dust mite (HDM) antigen and whether the allergic disease process could be worsened with repeated allergen exposure. In general, BN rats sensitized by either subcutaneous or intratracheal routes exhibited increased pulmonary allergy compared with Sprague-Dawley (SD) and Lewis (L) rats. Multiple intratracheal allergen exposures incrementally increased HDM-specific immune function in BN rats but progressively decreased eosinophil recruitment and markers of lung injury. SD rats had more moderate responses, whereas L rats were relatively unresponsive. Because BN rats developed stronger clinical hallmarks of allergic asthma under various immunization regimes compared with SD and L rats, we conclude that the BN is the most appropriate strain for studying allergic asthma-like responses in rats. Phenotypic differences in response to HDM were associated with differences in the Th1/Th2 cytokine balance and antioxidant capacity.
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Jo, Juandy, Johan Garssen, Leon Knippels, and Elena Sandalova. "Role of Cellular Immunity in Cow’s Milk Allergy: Pathogenesis, Tolerance Induction, and Beyond." Mediators of Inflammation 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/249784.
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Food allergy is an aberrant immune-mediated reaction against harmless food substances, such as cow’s milk proteins. Due to its very early introduction, cow’s milk allergy is one of the earliest and most common food allergies. For this reason cow’s milk allergy can be recognized as one of the first indications of an aberrant inflammatory response in early life. Classically, cow’s milk allergy, as is true for most other allergies as well, is primarily associated with abnormal humoral immune responses, that is, elevation of specific immunoglobulin E levels. There is growing evidence indicating that cellular components of both innate and adaptive immunity play significant roles during the pathogenesis of cow’s milk allergy. This is true for the initiation of the allergic phenotype (stimulation and skewing towards sensitization), development and outgrowth of the allergic disease. This review discusses findings pertaining to roles of cellular immunity in allergic inflammation, and tolerance induction against cow’s milk proteins. In addition, a possible interaction between immune mechanisms underlying cow’s milk allergy and other types of inflammation (infections and noncommunicable diseases) is discussed.
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Carlsten, Chris, Anders Blomberg, Mandy Pui, Thomas Sandstrom, Sze Wing Wong, Neil Alexis, and Jeremy Hirota. "Diesel exhaust augments allergen-induced lower airway inflammation in allergic individuals: a controlled human exposure study." Thorax 71, no. 1 (November 16, 2015): 35–44. http://dx.doi.org/10.1136/thoraxjnl-2015-207399.
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RationaleTraffic-related air pollution has been shown to augment allergy and airway disease. However, the enhancement of allergenic effects by diesel exhaust in particular is unproven in vivo in the human lung, and underlying details of this apparent synergy are poorly understood.ObjectiveTo test the hypothesis that a 2 h inhalation of diesel exhaust augments lower airway inflammation and immune cell activation following segmental allergen challenge in atopic subjects.Methods18 blinded atopic volunteers were exposed to filtered air or 300 µg PM2.5/m3 of diesel exhaust in random fashion. 1 h post-exposure, diluent-controlled segmental allergen challenge was performed; 2 days later, samples from the challenged segments were obtained by bronchoscopic lavage. Samples were analysed for markers and modifiers of allergic inflammation (eosinophils, Th2 cytokines) and adaptive immune cell activation. Mixed effects models with ordinal contrasts compared effects of single and combined exposures on these end points.ResultsDiesel exhaust augmented the allergen-induced increase in airway eosinophils, interleukin 5 (IL-5) and eosinophil cationic protein (ECP) and the GSTT1 null genotype was significantly associated with the augmented IL-5 response. Diesel exhaust alone also augmented markers of non-allergic inflammation and monocyte chemotactic protein (MCP)-1 and suppressed activity of macrophages and myeloid dendritic cells.ConclusionInhalation of diesel exhaust at environmentally relevant concentrations augments allergen-induced allergic inflammation in the lower airways of atopic individuals and the GSTT1 genotype enhances this response. Allergic individuals are a susceptible population to the deleterious airway effects of diesel exhaust.Trial registration numberNCT01792232.
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Chen, Yuwen, Hinayah Rojas de Oliveira, Amanda B. Alvarenga, Allan P. Schinckel, Terry S. Stewart, and Luiz F. Brito. "PSI-6 Genetic Parameters for Food Allergy Responses in Divergently-selected Pig Lines." Journal of Animal Science 99, Supplement_1 (May 1, 2021): 225–26. http://dx.doi.org/10.1093/jas/skab054.370.
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Abstract Genetic selection for health and welfare-related traits is paramount in livestock breeding. Piglet allergic responses to soybean protein negatively impact animal growth and welfare. The objectives of this study were to estimate the heritability of soybean allergic responses and genetic correlations between soybean and peanut allergies (r1,2) in divergently-selected pig lines. The base population consisted of nine sire lines (primarily Yorkshire and Landrace) and two dam sources (Yorkshire × Chester White-F1 and Landrace × Yorkshire-F1). Soybean and peanut-allergic responses were measured through a skin test (0–6 scale; 0-no allergic responses; 6-severe allergic responses; characterized by wheal and flair) on pigs fed a diet containing soybean meal for 21 d post-weaning. A total of 5,505 animals from nine generations of two contrasting lines (i.e., high and low skin test reaction) were included in the analyses. The statistical model included contemporary group, breeding lines, replication, sex, and weaning weight (linear covariate) as fixed effects (P-value < 0.05), and additive genetic, maternal genetic, and maternal permanent environment as random effects. Threshold and linear Bayesian models were used to estimate genetic parameters, using a pedigree-based relationship matrix containing 9,201 animals. The heritability estimates for the general soybean allergic response were 0.199 ± 0.045 and 0.119 ± 0.025 for the threshold (liability scale) and linear models, respectively, suggesting that soybean allergic responses are heritable and can be improved through selective breeding. A weak negative genetic correlation between allergic responses and birth weight was observed (r1,2 = -0.253 ± 0.192), which shows that the genetic variance of soybean allergy is less dependent on birth weight. However, a high positive genetic correlation was estimated between soybean and peanut-allergic responses (r1,2 = 0.89 ± 0.048), which indicates a potential cross-reactivity of soybean and peanut allergies. Our findings suggest that it is possible to reduce food allergy responses in pigs through selective breeding.
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Stelmaszczyk-Emmel, Anna, Anna Zawadzka-Krajewska, Eliza Głodkowska-Mrówka, and Urszula Demkow. "FoxP3 Tregs Response to Sublingual Allergen Specific Immunotherapy in Children Depends on the Manifestation of Allergy." Journal of Immunology Research 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/731381.
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Over the last decades allergic diseases has become a major health problem worldwide. The only specific treatment to date is allergen specific immunotherapy (ASIT). Although it was shown that ASIT generates allergen-tolerant T cells, detailed mechanism underlying its activity is still unclear and there is no reliable method to monitor its effectiveness. The aim of our study was to evaluate ASIT influence on the frequency of forkhead box P3 (FoxP3) Tregs in allergic children with various clinical manifestations. The relative number of FoxP3 Tregs in 32 blood samples from allergic children at baseline and/or after 1 year of ASIT was assessed by flow cytometry. In the entire studied group, the percentage of FoxP3 Tregs did not increase 1 year after ASIT. Nevertheless, the percentage of FoxP3 Tregs after ASIT significantly increased in children with respiratory allergy (conjunctivitis, asthma, and rhinitis) coexisting with nonrespiratory manifestations (food allergy and/or atopic dermatitis), whereas, in patients with respiratory allergy only, the percentage of FoxP3 Tregs decreased. To the best of our knowledge, this is the first report showing various differential FoxP3 Tregs response to ASIT in allergic children. FoxP3 Tregs number could be useful in treatment monitoring. Further studies are warranted to confirm these observations.
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Assa’ad, Amal H. "Oral food challenges." Journal of Food Allergy 2, no. 1 (September 1, 2020): 31–34. http://dx.doi.org/10.2500/jfa.2020.2.200008.
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Oral food challenge (OFC) is a procedure that is conducted most commonly by allergist/immunologists in their office or in food allergy centers to confirm a food allergy or to confirm tolerance to the food. The procedure as conducted in clinical practice is mostly open food challenge and, in research, a double-blind, placebo controlled food challenge. OFC has associated risks that can be minimized by having the challenges conducted by trained personnel who are prepared to treat allergic reactions and who have rescue medications available. However, OFCs have tremendous benefits to the patients and their families, including the potential to determine that a food is no longer an allergen and can be introduced into the diet. Even OFCs that result in clinical reactions have the benefit of confirming the food allergy and demonstrating the therapeutic effect of the rescue medications. The study of the outcomes of OFC has shed light on food allergy reactions and characteristics of the patients with food allergy as well as on the value of other diagnostic tests compared with OFC. OFCs have helped establish food allergy thresholds, confirm that subjects enrolled in research studies have the allergy, and demonstrate the response to the therapies tested in terms of ameliorating the allergic response or raising the reaction threshold. OFCs have also been used to promote the recent guidelines for the prevention of peanut allergy by identifying the infants at risk for peanut allergy but who are not allergic yet.
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Raftu, Gheorghe, Geta Mitrea, Luana Andreea Macovei, and Aurel Nechita. "Chemical Additives from the Composition of Plastic Products and Other Materials in Establishing Diagnosis for Alergy Disease." Materiale Plastice 55, no. 4 (December 30, 2018): 609–12. http://dx.doi.org/10.37358/mp.18.4.5085.
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Many of the chemical additives in the plastic products, besides the possible safety problems that may arise during the production process, have negative effecty, too, on the environment and human health. Plastic is a synthetic polymer. The polymers include starch, latex and cellulose, combined with different substances and chemicals, used in various formulas, the polymer is included in the naylon. At high temperatures such as microwave oven temperature, polymers can migrate from the packaging plastic in food. In most cases, establishing the diagnosis of allergic disease is a complex and difficult operation. This difficulty is primarily related to the polymorphism of the clinical manifestations accompanying allergic reactions, the existence during the evolution of these conditions, of long clinical asymptomatic latencies, as well as due to numerous subjective and objective symptoms that overlap with those caused by the allergen, complicating and altering the clinical picture. Allergies are an abnormal reaction of the body to allergens and develop in two stages. After the first contact with the allergen, the IgE antibodies are produced, and the second contact produces the allergic reaction. The produced antibodies will release the chemical mediators (histamine, prostaglandine, etc.) which cause an inflammatory response, vascular changes and irritation of the tissues, with the appearance of symptoms specific to allergy: redness, rash, itching, edema, etc.The so complex symptom of allergic diseases comprises several systems and organs at the same time, and the existence of over-additive phenomena makes it impossible to have characteristic clinical symptoms of allergic diseases that allow their identification only by clinical examination. However, this does not mean that the clinical exam and the analysis of the various objective and subjective symptoms presented by the patient is of no importance in establishing the diagnosis and recognizing the allergic character of the disease.The study includes a number of patients studied at the Galati Allergy Clinic. Specific immunotherapy known as desensitization or anti-allergic vaccination, is designed to fight the causes of allergies that occur when the immune system misinterprets harmless substances. Clinical examination results are complemented by allergen and specific antibody research; skin tests are the most common method for allergen detection.
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Chung, Sangwoon, Yong Gyu Lee, Manjula Karpurapu, Joshua A. Englert, Megan N. Ballinger, Ian C. Davis, Gye Young Park, and John W. Christman. "Depletion of microRNA-451 in response to allergen exposure accentuates asthmatic inflammation by regulating Sirtuin2." American Journal of Physiology-Lung Cellular and Molecular Physiology 318, no. 5 (May 1, 2020): L921—L930. http://dx.doi.org/10.1152/ajplung.00457.2019.
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The incidence of asthma has increased from 5.5% to near 8% of the population, which is a major health concern. The hallmarks of asthma include eosinophilic airway inflammation that is associated with chronic airway remodeling. Allergic airway inflammation is characterized by a complex interplay of resident and inflammatory cells. MicroRNAs (miRNAs) are small noncoding RNAs that function as posttranscriptional modulators of gene expression. However, the role of miRNAs, specifically miR-451, in the regulation of allergic airway inflammation is unexplored. Our previous findings showed that oxidant stress regulates miR-451 gene expression in macrophages during an inflammatory process. In this paper, we examined the role of miR-451 in regulating macrophage phenotype using an experimental poly-allergenic murine model of allergic airway inflammation. We found that miR-451 contributes to the allergic induction of CCL17 in the lung and plays a key role in proasthmatic macrophage activation. Remarkably, administration of a Sirtuin 2 (Sirt2) inhibitor diminished alternate macrophage activation and markedly abrogated triple-allergen [dust mite, ragweed, Aspergillus fumigatus (DRA)]-induced lung inflammation. These data demonstrate a role for miR-451 in modulating allergic inflammation by influencing allergen-mediated macrophages phenotype.
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Dona, Dulashi Withanage, and Cenk Suphioglu. "Egg Allergy: Diagnosis and Immunotherapy." International Journal of Molecular Sciences 21, no. 14 (July 16, 2020): 5010. http://dx.doi.org/10.3390/ijms21145010.
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Hypersensitivity or an allergy to chicken egg proteins is a predominant symptomatic condition affecting 1 in 20 children in Australia; however, an effective form of therapy has not yet been found. This occurs as the immune system of the allergic individual overreacts when in contact with egg allergens (egg proteins), triggering a complex immune response. The subsequent instantaneous inflammatory immune response is characterized by the excessive production of immunoglobulin E (IgE) antibody against the allergen, T-cell mediators and inflammation. Current allergen-specific approaches to egg allergy diagnosis and treatment lack consistency and therefore pose safety concerns among anaphylactic patients. Immunotherapy has thus far been found to be the most efficient way to treat and relieve symptoms, this includes oral immunotherapy (OIT) and sublingual immunotherapy (SLIT). A major limitation in immunotherapy, however, is the difficulty in preparing effective and safe extracts from natural allergen sources. Advances in molecular techniques allow for the production of safe and standardized recombinant and hypoallergenic egg variants by targeting the IgE-binding epitopes responsible for clinical allergic symptoms. Site-directed mutagenesis can be performed to create such safe hypoallergens for their potential use in future methods of immunotherapy, providing a feasible standardized therapeutic approach to target egg allergies safely.
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Neha Sharma, Shuchi Kaushik, and Rajesh Singh Tomar. "Prediction of the allergic response of extracellular amylase producing bacteria through in-silico method." International Journal of Research in Pharmaceutical Sciences 10, no. 2 (April 14, 2019): 1185–89. http://dx.doi.org/10.26452/ijrps.v10i2.404.
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Allergies intolerance is a common problem worldwide. The major difficulties are related to the correct diagnosis of causes which is associated with amino acid sequences present in the epitope region of allergen. So there is a need to find out the factors causing allergies and allergens themselves. In the present study a bioinformatics tool is used to predict amino acid sequence and mast cell association with different integrated approaches. Internet databases for amylase producing bacteria were used in In-silico method to check the allergy for microorganism producing the extracellular enzyme. Amylase is an extracellular enzyme isolated from soil bacteria Salmonella species and Proteus vulgaris. It is very important in the pharmaceutical industry to check the allergenicity of any drug, protein or enzyme that be used in the treatment of diseases or food industries for various purpose. The aim of the present study is isolation and characterisation of extracellular enzyme produced from soil bacteria and to analyzed allergic response through AlgPred tool of bioinformatics. From results, it was concluded that the protein sequence of amylase did not contain any epitope, no hits for mast and blast which proved that it was not an allergen. So, bacterial isolates from the industrial soil are a good alternative source of enzyme production and may be used as an industrial level. Thus, from the results, it may be concluded that microbes from soil sample can be a good source of industrially important enzymes without any allergy.
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Nair, Bindukumar, John C. Wheeler, Donald E. Sykes, Paula Brown, Jessica L. Reynolds, Ravikumar Aalinkeel, Supriya D. Mahajan, and Stanley A. Schwartz. "Proteomic Approach to Evaluate Mechanisms That Contribute to Food Allergenicity: Comparative 2D-DIGE Analysis of Radioallergosorbent Test Positive and Negative Patients." International Journal of Proteomics 2011 (September 19, 2011): 1–13. http://dx.doi.org/10.1155/2011/673618.
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Proteomic profiles of RAST+ subjects with severe food allergies and RAST− subjects were compared using 2D-DIGE analysis to obtain candidate biomarkers specific to food allergies. Our analysis highlighted 52 proteins that were differentially expressed between the RAST+ and RAST− groups of which 37 were successfully identified that include chondroitin sulfates, zinc finger proteins, C-type lectins, retinoic acid binding proteins, heat shock proteins, myosin, cytokines, mast cell expressed proteins, and MAP kinases. Biological network analysis tool Metacore revealed that most of these regulated proteins play a role in immune tolerance, hypersensitivity and modulate cytokine patterns inducing a Th2 response that typically results in IgE-mediated allergic response which has a direct or indirect biological link to food allergy. Identifying unique biomarkers associated with certain allergic phenotypes and potentially cross-reactive proteins through bioinformatics analyses will provide enormous insight into the mechanisms that underlie allergic response in patients with food allergies.
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Cardoso, Cristina R., Pauline R. Provinciatto, Dannielle F. Godoi, Beatriz R. Ferreira, Gerlinde Teixeira, Marcos A. Rossi, Fernando Q. Cunha, and João S. Silva. "IL-4 regulates susceptibility to intestinal inflammation in murine food allergy." American Journal of Physiology-Gastrointestinal and Liver Physiology 296, no. 3 (March 2009): G593—G600. http://dx.doi.org/10.1152/ajpgi.90431.2008.
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Allergies involve a state of immediate hypersensitivity to antigens, including food proteins. The mechanism underlying the initiation and development of allergic responses involves IL-4 that directly induces the differentiation of committed effector Th2 lymphocytes. Although it is clear that Th2 responses play a pivotal role in the development of allergic responses, it remains unclear which mechanisms are involved in the development of the intestinal damages observed in food allergy. Accordingly, this work aimed to study the role of Th2/IL-4-dependent responses in the development of food allergy and intestinal pathology. C57BL/6 wild-type (WT) and IL-4−/− mice were sensitized with peanut proteins, challenged with peanut seeds, and followed for the development of food allergy and intestinal inflammation. Results demonstrated that exposure to peanut seeds led to weight loss in WT but not in IL-4−/− mice that preserved gut integrity with no signs of mucosal inflammation. These animals presented increased levels of IgG2a in sera, suggesting a role for allergic antibodies in the pathogenesis of WT animals. Most importantly, results also showed that lack of IL-4 modulated gut mucosal response in food allergy through diminished expression of TNF-α mRNA, increased Th1 IFN-γ, IL-12p40, regulatory cytokines, and Foxp3, demonstrating their relevance in the control of allergic inflammatory processes, especially in the intestine. Finally, this study highlighted some of the complex mechanisms involved in the pathogenesis of allergic responses to food antigens in the gut, thereby providing valuable tools for directing novel therapeutic or preventive strategies to the control of allergic enteropathy.
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Lew, D. Betty, Kim S. LeMessurier, Maneesha Palipane, Yanyan Lin, and Amali E. Samarasinghe. "Saccharomyces cerevisiae-Derived Mannan Does Not Alter Immune Responses to Aspergillus Allergens." BioMed Research International 2018 (2018): 1–9. http://dx.doi.org/10.1155/2018/3298378.
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Severe asthma with fungal sensitization predominates in the population suffering from allergic asthma, to which there is no cure. While corticosteroids are the mainstay in current treatment, other means of controlling inflammation may be beneficial. Herein, we hypothesized that mannan from Saccharomyces cerevisiae would dampen the characteristics of fungal allergic asthma by altering the pulmonary immune responses. Using wild-type and transgenic mice expressing the human mannose receptor on smooth muscle cells, we explored the outcome of mannan administration during allergen exposure on the pathogenesis of fungal asthma through measurement of cardinal features of disease such as inflammation, goblet cell number, and airway hyperresponsiveness. Mannan treatment did not alter most hallmarks of allergic airways disease in wild-type mice. Transgenic mice treated with mannan during allergen exposure had an equivalent response to non-mannan-treated allergic mice except for a prominent granulocytic influx into airways and cytokine availability. Our studies suggest no role for mannan as an inflammatory regulator during fungal allergy.
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Kitaoka, Momoko, Wei Xiao, Qingliang Kong, Yoshiro Tahara, Noriho Kamiya, and Masahiro Goto. "A Solid-in-Oil Nanodispersion System for Transcutaneous Immunotherapy of Cow’s Milk Allergies." Pharmaceutics 12, no. 3 (February 27, 2020): 205. http://dx.doi.org/10.3390/pharmaceutics12030205.
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An allergy to cow’s milk proteins is the most common food allergy in infants and toddlers. Conventional oral immunotherapy for cow’s milk allergies requires hospital admission due to the risk of severe allergic reactions, including anaphylaxis. Therefore, a simpler and safer immunotherapeutic method is desirable. We examined transcutaneous immunotherapy with a solid-in-oil (S/O) system. In the S/O system, nano-sized particles of proteins are dispersed in an oil-vehicle with the assistance of nonionic surfactants. In the present study, the S/O system enhanced the skin permeation of the allergen molecule β-lactoglobulin (BLG), as compared with a control PBS solution. The patches containing BLG in the S/O nanodispersion skewed the immune response in the allergy model mice toward T helper type 1 immunity, indicating the amelioration of allergic symptoms. This effect was more pronounced when the immunomodulator resiquimod (R-848) was included in the S/O system.
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Rakhmatullina, N. M., Yu V. Pastushenko, O. R. Trofimova, N. A. Sibgatullina, D. G. Akhmedzyanova, and G. N. Zakirov. "Modern methods of allergen-specific immunotherapy in allergic rhinitis treatment." Kazan medical journal 97, no. 2 (April 15, 2016): 288–94. http://dx.doi.org/10.17750/kmj2016-288.
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The article presents the modern methods of allergen-specific immunotherapy in patients with allergic rhinitis. Allergen-specific immunotherapy - a method of treating allergic diseases, involves reducing the organism’s sensitivity to the allergen effects by repeated administration of allergen extract, starting with the minimum dose. Given the allergic rhinitis high prevalence, as well as its tendency to increase, strong interest in effective methods of its treatment is fully justified. Over the last 20 years, it has become clear that asthma and rhinitis are two types of manifestations of a single pathological process in the airways. It has been proven that allergic disease clinical features may change over time. In addition, patients with allergy are prone to multivalent sensitization. Currently none of the drugs used to relieve allergic rhinitis symptoms can not change the organism’s response to an allergen. Allergen-specific immunotherapy can reduce allergic disease symptoms severity, reduces the need in drugs use, decreases the chance of additional sensitization to other allergens, prevents the asthma development. This therapy has become one of the most widely used effective methods of atopic diseases treatment: seasonal and perennial rhinoconjunctivitis, atopic asthma. Allergen-specific immunotherapy can lead to a change in the immunological response to the relevant allergens in early stages, acting through regulatory cells. Current studies are aimed, on the one hand, at reducing the therapeutic allergovaccines ability to cause allergic reactions, on the other - to maintain or enhance their immunogenic properties. Achieving this goal is possible by changing the route of administration and delivery of therapeutic allergens (non-injection methods of allergen-specific immunotherapy), and using a variety of allergens modification techniques.
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Jacquet, Alain. "New Insights into the Molecular Basis of the House Dust Mite-Induced Allergic Response." Open Allergy Journal 2, no. 1 (July 13, 2009): 38–44. http://dx.doi.org/10.2174/1874838400902010038.
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House dust mite (HDM) represents world-wide one of the most common source of aeroallergens word-wide and more than 50% of allergic patients are sensitized to these allergenic molecules. Although the induction of specificTh2 cells as well as IgE by HDM is well understood, the events that control the initial Th2 polarization in response to HDM are still poorly defined. Notably, mechanisms by which HDM is recognized by the airway mucosa, interacts with barrier epithelial cells, leading to dendritic cell (DC) recruitment, activation, and subsequent Th2-mediated responses, remains to be elucidated. Moreover, whereas the allergenicity of the group 1 major mite allergens could be largely explained by their intrinsic proteolytic activity, the fundamental mechanistic question regarding the putative intrinsic allergenic properties of the group 2 major mite allergen remained unanswered to date. This review summarizes new insights into diverse determinants that contribute to the HDM allergenicity. In addition to the auto-adjuvant capacity of the two major mite allergen Der p 1 and 2, due to proteolytic activity and functional mimicry of the Toll-like receptor 4 (TLR4) co-receptor MD2 respectively, contaminating factors derived from HDM carriers, mainly endotoxins (LPS) et β-glucans, are very important to activate the innate immune response which, in turns, is involved in the development of allergic response by HDM.
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Lariou, Maria Stella, Stavroula Dikalioti, Nick Dessypris, Apostolos Pourtsidis, Margarita Baka, Sophia Polychronopoulou, Fani Athanasiadou Piperopoulou, et al. "Country specific serum IgE reactivity profile and concordance with allergic history among acute lymphoblastic leukemia children and controls." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): e20002-e20002. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e20002.
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e20002 Background: Allergy has been studied as a risk factor for several malignancies, including childhood leukemia; yet, the tentative etiological nature of this association needs to be further explored. Published studies suffer inappropriate study design and accuracy of exposure variables. In response to the latter need, this study aims to use country specific biological markers, namely levels of the most prevalent allergen-specific immunoglobulin E (IgE) antibodies in Greece as an alternative exposure measurement to history of allergy and compare their concordance with allergic history. Methods: Allergen-specific-IgEs against 24 most prevalent inhalant and food allergens were determined for 199 incident childhood acute lymphoblastic leukemia (ALL), newly diagnosed cases across Greece and registered in the Nationwide Registry for Childhood Hematological Malignancies (NARECHEM) and 113 hospital controls. K statistic was used to check the concordance between serum IgE specific allergens and allergic history overall, as well as among cases and controls. Results: Concordance between self-reported food allergy and food IgE levels in the same individual among both cases and controls was 87% and 83% for respiratory allergens. Among cases, concordance between self reported food allergies and food IgEs was 92% and 80% for controls (p-value 0.003) and the respective κ statistics were 0.28 for cases and 0.10 for controls. Concordance between self reported respiratory allergies and respiratory IgEs was 84% for cases and 81% for controls (p-value 0.57); κ statistics 0.09 for cases and 0.07 for controls. Conclusions: Much of the discordance among cases and controls (self-report false positives) might probably be a reflection of non allergic food hypersensitivity, an allergy that was surpassed or extended allergen avoidance. Other discordance (self-report false negatives) seems to be the result of food sensitization, either hypoclinical or not acknowledged as a type of allergy by mothers of the children. Nevertheless, these measurements jointly analyzed are valuable in exploring the stated hypothesis, especially in well designed prospective studies.
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Petalas, K., and S. R. Durham. "Allergen immunotherapy for allergic rhinitis." Rhinology journal 51, no. 2 (June 1, 2013): 99–110. http://dx.doi.org/10.4193/rhino12.086.
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Allergic rhinitis, a risk factor for bronchial asthma, is a global health problem that impairs patients` physical and social activity and consequently their quality of life. Specific Immunotherapy (SIT) involves the administration, subcutaneously or sublingually, of increasing doses of the causative allergen, in order to induce clinical and immunologic tolerance. SIT has been shown to be effective in those with a poor response to conventional drug therapy. Immunotherapy has been shown to have disease-modifying effects and result in long term remission of allergic symptoms and reduces the risk of progression from rhinitis to asthma, as well as the chances of developing new sensitizations to allergens. Injection immunotherapy is a safe treatment for allergic rhinitis with/without mild controlled asthma, provided that it is performed in the context of a harmonious interaction between trained medical personnel and appropriately selected patients. Immunotherapy suppresses early and late responses to allergen exposure by modifying both T-cell and B-cell responses to inhaled allergens. Immune deviation of allergen-specific T cell responses in favour of Th1 and/or the induction of regulatory T cells is crucial in achieving immune tolerance. Increased understanding of the mechanisms of immunotherapy has identified potential biomarkers of the response to treatment and highlighted new therapeutic pathways with potential for even more effective future standardized vaccines.
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Rowane, Marija, Ryan Shilian, Devi K. Jhaveri, Haig H. Tcheurekdjian, Theordore H. Sher, and Robert Hostoffer. "Familial Success in Allergen Desensitization." Allergy & Rhinology 10 (January 2019): 215265671989031. http://dx.doi.org/10.1177/2152656719890315.
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Introduction Allergic rhinitis (AR) is a widely prevalent immunoglobulin E-mediated inflammatory nasal condition resulting from reexposure to an allergen in a sensitized individual. The genetic associations behind AR and other allergic conditions have been studied. However, familial success with AR therapies, specifically allergen desensitization through subcutaneous immunotherapy (SCIT), has never been reported in the literature. Pharmocogenetics has been gradually applied to link heritable genetic variants with drug responses, such as intergenic region variants APOBEC3B and APOBEC3C and β2-adrenergic receptor and glycoprotein ADAM33 polymorphisms as predictive biomarkers for biologic treatment response in asthma. We provide the first reported survey of familial success with SCIT. Methods We administered a month-long, institutional review board-approved (20190493) questionnaire to 200 adult patients receiving SCIT in a suburban allergy/immunology practice. The anonymous survey inquired about demographics, target allergens for their SCIT, current symptom improvement on SCIT, and family history of allergies and SCIT management. Results Twenty-six percent (52 of 200, 26%) SCIT patients reported familial success with the same allergy treatment modality. AR diagnosis and symptom improvement from SCIT was similar among previous/same (18 of 52, 38%; 26 of 52, 54%) and subsequent (10 of 52, 21%; 19 of 52, 40%) generations of family members. A combination of seasonal and perennial allergies was most prevalent (81%) among this population. Conclusion In a subpopulation of SCIT patients, there appears to be a familial success rate with this allergen desensitization treatment. This is the first reported pharmocogenetic evidence of assessing hereditary influence on effective AR therapy. Understanding pharmacogenetic associations involved with SCIT may improve allergists’ recommendations for this treatment option.
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Calzada, David, Lucía Cremades-Jimeno, María López-Ramos, and Blanca Cárdaba. "Peptide Allergen Immunotherapy: A New Perspective in Olive-Pollen Allergy." Pharmaceutics 13, no. 7 (July 2, 2021): 1007. http://dx.doi.org/10.3390/pharmaceutics13071007.
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Allergic diseases are highly prevalent disorders, mainly in industrialized countries where they constitute a high global health problem. Allergy is defined as an immune response “shifted toward a type 2 inflammation” induced by the interaction between the antigen (allergen) and IgE antibodies bound to mast cells and basophils that induce the release of inflammatory mediators that cause the clinical symptoms. Currently, allergen-specific immunotherapy (AIT) is the only treatment able to change the course of these diseases, modifying the type 2 inflammatory response by an allergenic tolerance, where the implication of T regulatory (Treg) cells is considered essential. The pollen of the olive tree is one of the most prevalent causes of respiratory allergic diseases in Mediterranean countries, inducing mainly nasal and conjunctival symptoms, although, in areas with a high antigenic load, olive-tree pollen may cause asthma exacerbation. Classically, olive-pollen allergy treatment has been based on specific immunotherapy using whole-olive pollen extracts. Despite extracts standardization, the effectiveness of this strategy varies widely, therefore there is a need for more effective AIT approaches. One of the most attractive is the use of synthetic peptides representing the B- or T-cell epitopes of the main allergens. This review summarizes experimental evidence of several T-cell epitopes derived from the Ole e 1 sequence to modulate the response to olive pollen in vitro, associated with several possible mechanisms that these peptides could be inducing, showing their usefulness as a safe preventive tool for these complex diseases.
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Siddall, Hilary, Diana Quint, Hitesh Pandya, Will Powley, Shaila Shabbir, Jens M. Hohlfeld, Dave Singh, and Laurie Lee. "Intranasal GSK2245035, a Toll-like receptor 7 agonist, does not attenuate the allergen-induced asthmatic response in a randomized, double-blind, placebo-controlled experimental medicine study." PLOS ONE 15, no. 11 (November 9, 2020): e0240964. http://dx.doi.org/10.1371/journal.pone.0240964.
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Background Allergic asthma is a heterogenous disorder predominantly driven by a type 2 inflammatory response to aeroallergens. Therapeutic modulation to rebalance these type 2 responses may offer clinical benefit for allergic respiratory inflammatory diseases, with the potential for disease modification. GSK2245035, a selective toll-like receptor-7 agonist, preferentially stimulates the induction of type 1 interferon alpha, reducing type 2 responses. Objective This study investigated whether intranasal GSK2245035 reduced allergen-induced bronchial reactivity in mild allergic asthma. Methods This double-blind, placebo-controlled, parallel-group Phase IIa trial randomized (1:1) participants with mild allergic asthma to intranasal GSK2245035 20 ng or placebo once weekly for 8 weeks; follow-up was conducted 1, 4, and 12 weeks after treatment. Allergen-induced late asthmatic response 1 week after treatment was measured as minimum and weighted mean forced expiratory volume in 1 second (FEV1) 4–10 hours following bronchial allergen challenge (primary endpoint). Pharmacodynamic and allergic biomarkers, and adverse events, were assessed. A Bayesian analysis framework was used; a posterior probability >0.7 denoted primary endpoint success. Results Thirty-six participants were randomized (GSK2245035, n = 22; placebo, n = 14). The percentage attenuation in late asthmatic response was –4.6% (posterior probability: 0.385) and –10.5% (posterior probability: 0.303) for minimum and weighted mean FEV1, respectively. Type 2 responses were confirmed by changes in lung function, eosinophils (blood and sputum), interleukin-5 (sputum) and fractional exhaled nitric oxide biomarkers pre- and post-bronchial allergen challenge. However, no treatment effect was observed. Adverse events were reported by 10/14 (71%) and 21/22 (95%) participants in the placebo and GSK2245035 groups, respectively; headache was the most common. Conclusions and clinical relevance Although target engagement was observed, weekly intranasal GSK2245035 20 ng for 8 weeks did not substantially attenuate the late asthmatic response in participants with mild allergic asthma. Overall, treatment was well tolerated.
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Wilson, Mark S., Matthew D. Taylor, Adam Balic, Constance A. M. Finney, Jonathan R. Lamb, and Rick M. Maizels. "Suppression of allergic airway inflammation by helminth-induced regulatory T cells." Journal of Experimental Medicine 202, no. 9 (November 7, 2005): 1199–212. http://dx.doi.org/10.1084/jem.20042572.
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Allergic diseases mediated by T helper type (Th) 2 cell immune responses are rising dramatically in most developed countries. Exaggerated Th2 cell reactivity could result, for example, from diminished exposure to Th1 cell–inducing microbial infections. Epidemiological studies, however, indicate that Th2 cell–stimulating helminth parasites may also counteract allergies, possibly by generating regulatory T cells which suppress both Th1 and Th2 arms of immunity. We therefore tested the ability of the Th2 cell–inducing gastrointestinal nematode Heligmosomoides polygyrus to influence experimentally induced airway allergy to ovalbumin and the house dust mite allergen Der p 1. Inflammatory cell infiltrates in the lung were suppressed in infected mice compared with uninfected controls. Suppression was reversed in mice treated with antibodies to CD25. Most notably, suppression was transferable with mesenteric lymph node cells (MLNC) from infected animals to uninfected sensitized mice, demonstrating that the effector phase was targeted. MLNC from infected animals contained elevated numbers of CD4+CD25+Foxp3+ T cells, higher TGF-β expression, and produced strong interleukin (IL)-10 responses to parasite antigen. However, MLNC from IL-10–deficient animals transferred suppression to sensitized hosts, indicating that IL-10 is not the primary modulator of the allergic response. Suppression was associated with CD4+ T cells from MLNC, with the CD4+CD25+ marker defining the most active population. These data support the contention that helminth infections elicit a regulatory T cell population able to down-regulate allergen induced lung pathology in vivo.
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Zhao, Xiaoli, Suzan Thijssen, Hongbing Chen, Johan Garssen, Leon M. J. Knippels, and Astrid Hogenkamp. "Selenium Modulates the Allergic Response to Whey Protein in a Mouse Model for Cow’s Milk Allergy." Nutrients 13, no. 8 (July 22, 2021): 2479. http://dx.doi.org/10.3390/nu13082479.
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Cow’s milk allergy is a common food allergy in infants, and is associated with an increased risk of developing other allergic diseases. Dietary selenium (Se), one of the essential micronutrients for humans and animals, is an important bioelement which can influence both innate and adaptive immune responses. However, the effects of Se on food allergy are still largely unknown. In the current study it was investigated whether dietary Se supplementation can inhibit whey-induced food allergy in an animal research model. Three-week-old female C3H/HeOuJ mice were intragastrically sensitized with whey protein and cholera toxin and randomly assigned to receive a control, low, medium or high Se diet. Acute allergic symptoms, allergen specific immunoglobulin (Ig) E levels and mast cell degranulation were determined upon whey challenge. Body temperature was significantly higher in mice that received the medium Se diet 60 min after the oral challenge with whey compared to the positive control group, which is indicative of impaired anaphylaxis. This was accompanied by reductions in antigen-specific immunoglobulins and reduced levels of mouse mast cell protease-1 (mMCP-1). This study demonstrates that oral Se supplementation may modulate allergic responses to whey by decreasing specific antibody responses and mMCP-1 release.
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Pérez-Gómez, Cristina, José M. Segura, Miguel Blanca, Maite Asenjo, and José M. Matés. "Antioxidant activity levels and oxidative stress as blood markers of allergic response to drugs." Biochemistry and Cell Biology 78, no. 6 (December 1, 2000): 691–98. http://dx.doi.org/10.1139/o00-085.
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Antioxidant enzymes work together in human blood cells against toxic reactive oxygen species. Although their relationship with several pathophysiologic processes has been stated, not much is known about the connection between antioxidant defence and allergy. This study was designed to determine the enzymatic activities and the oxidative indices in the blood and serum proteins in patients suffering from allergy to drugs. We hypothesize that serum and blood reactions may serve as useful clinical marker for the allergic state. We used enzymatic antioxidant activities, thiobarbituric acid reactive substances, and carbonyl contents of proteins as suitable markers. We determined superoxide dismutases, glutathione peroxidase and catalase activities in each cell type. After antihistaminics plus steroids were given as part of a protocol treatment, enzymatic antioxidant activities, thiobarbituric acid reactive substance levels, and carbonyl contents were used as recovering markers for the disease. We found a relationship between antioxidant enzymatic activities, thiobarbituric acid reactive substance levels, and carbonyl contents for allergic reactions belonging to several type I and type IV allergies, as well as cross-reactive intolerance to nonsteroidal anti-inflammatory drugs and an anaphylactoid reaction to a radiocontrast media. A similar pattern also exists for analogous allergic manifestations and disease-like status.Key words: allergy, blood, catalase, glutathione peroxidase, superoxide dismutase.
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Papia, Francesco, Chiara Bellia, and Carina Gabriela Uasuf. "Tropomyosin: A panallergen that causes a worldwide allergic problem." Allergy and Asthma Proceedings 42, no. 5 (September 1, 2021): e145-e151. http://dx.doi.org/10.2500/aap.2021.42.210057.
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Background: Panallergens are proteins that take part in key processes of organisms and, therefore, are ubiquitously distributed with highly conserved sequences and structures. One class of these panallergens is composed of the tropomyosins. The highly heat-stable tropomyosins comprise the major allergens in crustaceans and mollusks, which make them important food allergens in exposed populations. Tropomyosins are responsible for a widespread immunoglobulin E cross-reactivity among allergens from different sources. Allergic tropomyosins are expressed in many species, including parasites and insects. Methods: This panallergen class is divided, according to it capacity of induced allergic symptoms, into allergenic or nonallergenic tropomyosin. Although vertebrate tropomyosins share ∼55% of sequence homology with invertebrate tropomyosins, it has been thought that the invertebrate tropomyosins would not have allergic properties. Nevertheless, in recent years, this opinion has been changed. In particular, tropomyosin has been recognized as a major allergen in many insects. Results: A high grade of homology has been shown among tropomyosins from different species, such as crustaceans and insects, which supports the hypothesis of cross-reactivity among tropomyosins from divergent species. Moreover, the emerging habit of consuming edible insects has drawn the attention of allergists to invertebrate tropomyosin protein due to its potential allergenic risk. Nevertheless, evidence about tropomyosin involvement in clinical allergic response is still scarce and deserves more investigation. Conclusion: This review intended to report allergic reactions associated with different tropomyosins when considering house dust mites, parasites, seafood, and insects, and to summarize our current knowledge about its cross-reactivity because this could help physicians to accurately diagnose patients with food allergy.
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Saliganti, Vamshi, Rajeev Kapila, Rohit Sharma, and Suman Kapila. "Feeding probiotic Lactobacillus rhamnosus (MTCC 5897) fermented milk to suckling mothers alleviates ovalbumin-induced allergic sensitisation in mice offspring." British Journal of Nutrition 114, no. 8 (September 2, 2015): 1168–79. http://dx.doi.org/10.1017/s000711451500286x.
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AbstractThe neonatal period is often polarised to T helper (Th2) response at the time of birth, predisposing offspring to allergic disorders. Passive immunity through the mother’s milk is critical for immune system development of newborns. Probiotics have been proposed to harmonise Th1/Th2 imbalance in allergic conditions in adults. In the present study, the anti-allergic effects of feeding probiotic Lactobacillus rhamnosus-fermented milk (PFM) either to dams during the suckling period or to their offspring after weaning individually or else in successive periods against ovalbumin (OVA)-induced allergy in newborns was analysed. After allergen sensitisation, physical symptoms of allergy, gut immune response, humoral immune response and cell-mediated response through interleukins were detected. Consumption of PFM by mothers and offspring showed a reduction (P<0·01) in physical allergic symptoms in newborns with an increase (P<0·01) in the numbers of goblet and IgA+ cells in the small intestine. Similarly, considerable (P<0·001) decreases in OVA-specific antibodies (IgE, IgG, IgG1) and ratios of IgE/IgG2a and IgG1/IgG2a in the sera of newborn mice were recorded. A decrease in IL-4 and an increase in interferon-γ levels further confirmed the shift from Th2 to Th1 pathway in PFM-fed mice. It is logical to conclude that the timing of PFM intervention in alleviating allergic symptoms is critical, which was found to be most effective when mothers were fed during the suckling period.
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Msallam, Rasha, Jozef Balla, Abhay P. S. Rathore, Hassen Kared, Benoit Malleret, Wilfried A. A. Saron, Zhaoyuan Liu, et al. "Fetal mast cells mediate postnatal allergic responses dependent on maternal IgE." Science 370, no. 6519 (October 29, 2020): 941–50. http://dx.doi.org/10.1126/science.aba0864.
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Mast cells (MCs) are central effector cells in allergic reactions that are often mediated by immunoglobulin E (IgE). Allergies commonly start at an early age, and both MCs and IgE are detectable in fetuses. However, the origin of fetal IgE and whether fetal MCs can degranulate in response to IgE-dependent activation are presently unknown. Here, we show that human and mouse fetal MCs phenotypically mature through pregnancy and can be sensitized by maternal IgE. IgE crossed the placenta, dependent on the fetal neonatal Fc receptor (FcRN), and sensitized fetal MCs for allergen-specific degranulation. Both passive and active prenatal sensitization conferred allergen sensitivity, resulting in postnatal skin and airway inflammation after the first allergen encounter. We report a role for MCs within the developing fetus and demonstrate that fetal MCs may contribute to antigen-specific vertical transmission of allergic disease.
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Gushchin, I. S. "Transepithelial initiation of allergic response." Russian Journal of Allergy 13, no. 3 (December 15, 2016): 3–10. http://dx.doi.org/10.36691/rja346.
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Furrie, Elizabeth. "Probiotics and allergy." Proceedings of the Nutrition Society 64, no. 4 (November 2005): 465–69. http://dx.doi.org/10.1079/pns2005466.
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Allergy is caused by an immune reaction that is out of all proportion to the antigenic stimuli. Classical allergy is a type I hypersensitivity reaction mediated by the interaction of mast cells (and eosinophils) coated with allergen-specific IgE and a cross-linking allergen. The physiological outcome is inflammation commonly displayed by urticaria, rhinitis, vomiting and diarrhoea, depending on the route of allergen entry. In extreme reactions anaphylactic shock can result that may lead to death. Chronic allergic responses most commonly present themselves as asthma and eczema. All these symptoms are the consequence of an imbalanced immune system making an unsuitable response to an environmental or food antigen. On bacterial colonisation of the colon after birth the appropriate microbiological stimuli is essential to redress the balance of the skewed T-helper 2 immune response present in the newborn. This normal interaction between baby and microbes is thought to be compromised in the Western world, with a reduction in bifidobacteria and an increase in clostridial species, particularly in bottle-fed infants. The use of probiotic therapy to prevent allergic disease has been demonstrated in two studies using a probiotic Lactobacillus rhamnosus GG in neonates. A long-term reduction in allergy has been shown in the test group, with lactobacillus reducing the incidence of atopic eczema. Management of allergy through probiotics has also been demonstrated in infants, using lactobacilli to control atopic eczema and cow's milk allergy. Unfortunately, these positive results have not been repeated in studies with older children and young adults.
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Arcimowicz, Magdalena, and Edyta Krzych-Fałta. "Nasal allergen challenge - an important tool in diagnosis of rhinologic disease." Polski Przegląd Otorynolaryngologiczny 9, no. 4 (December 19, 2020): 1–5. http://dx.doi.org/10.5604/01.3001.0014.6068.
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The nasal allergen challenge (NAC) is used in the diagnosis of rhinitis. The primary use of NAC is to confirm allergy to a specific inhaled allergen. NAC reproduces the allergic reaction of the nasal mucosa under standardized and controlled conditions that occurs after direct intranasal administration of allergens. As the only used method for assessing the degree of allergy, it mimics the body’s natural response to the sensitizing factor in the early and late stages of an allergic reaction. NAC is used in the diagnosis of chronic, occupational and local rhinitis, as well as in the differential diagnosis of rhinitis and ophthalmic symptoms. Under conditions similar to natural exposure, it determines the relationship between the allergen and symptoms of allergic rhinitis, especially in the case of difficulties in interpreting the results of skin tests and the serum concentration of specific IgE. It is a truly valuable tool in determining the indications for immunotherapy and the selection of allergens for desensitization therapy. It also serves as a method of monitoring the effectiveness of immunotherapy and pharmacotherapy. For scientific purposes, NAC is used to study the mechanisms of an allergic reaction and the influence of various factors on its course. It is considered safe, but requires appropriate instruments and qualified personnel.
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Alashkar Alhamwe, Bilal, Laura A. P. M. Meulenbroek, Désirée H. Veening-Griffioen, Tjalling M. D. Wehkamp, Fahd Alhamdan, Sarah Miethe, Hani Harb, et al. "Decreased Histone Acetylation Levels at Th1 and Regulatory Loci after Induction of Food Allergy." Nutrients 12, no. 10 (October 19, 2020): 3193. http://dx.doi.org/10.3390/nu12103193.
Full textAbstract:
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.
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Cockcroft, Donald W., Fredrick E. Hargreave, Paul M. O’Byrne, and Louis-Philippe Boulet. "Understanding Allergic Asthma from Allergen Inhalation Tests." Canadian Respiratory Journal 14, no. 7 (2007): 414–18. http://dx.doi.org/10.1155/2007/753450.
Full textAbstract:
The allergen challenge has evolved, in less than 150 years, from a crude tool used to document the etiology of allergen-induced disease to a well-controlled tool used today to investigate the pathophysiology and pharmacotherapy of asthma. Highlights of the authors’ involvement with the allergen challenge include confirmation of the immunoglobulin E-dependence of the late asthmatic response, importance of (nonallergic) airway hyper-responsiveness as a determinant of the airway response to allergen, identification of allergen-induced increase in airway hyper-responsiveness, documentation of beta2-agonist-induced increase in airway response to allergen (including eosinophilic inflammation), advances in understanding the pathophysiology and kinetics of allergen-induced airway responses, and development of a muticentre clinical trial group devoted to using the allergen challenge for investigating promising new therapeutic strategies for asthma.
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Baroody, Fuad M., Samantha M. Mucha, Marcy deTineo, and Robert M. Naclerio. "Evidence of Maxillary Sinus Inflammation in Seasonal Allergic Rhinitis." Otolaryngology–Head and Neck Surgery 146, no. 6 (February 1, 2012): 880–86. http://dx.doi.org/10.1177/0194599811435972.
Full textAbstract:
Objective. Allergic rhinitis has been frequently associated with both acute and chronic sinusitis. Previous studies have shown an influx of eosinophils into the maxillary sinus after nasal challenge with allergen. The objective of this study was to determine, in humans, if the development of seasonal allergic inflammation, secondary to natural allergen exposure, leads to similar inflammation within the maxillary sinus. Study Design. Prospective, longitudinal study. Setting. Academic medical center and research laboratory. Subjects and Methods. Eighteen subjects were evaluated in and out of the ragweed allergy season using subjective measures (nasal symptoms, quality of life), nasal secretory response to methacholine challenge, and evaluation of biomarkers in nasal and sinus lavages. Results. The subjects became symptomatic during the season and reported worse quality of life and increased nasal reactivity to methacholine. The total number of eosinophils obtained by nasal lavage during the season (median= 35,691) was significantly higher compared with out of season (median = 2811, P ≤ .02). Similarly, there were significantly more eosinophils, albeit to a lesser magnitude, in the maxillary sinus during the season (median = 4248) compared with the out-of-season samples (median = 370, P ≤ .02). Conclusion. The authors provide evidence that natural exposure to pollen during an individual’s allergy season leads to both nasal and sinus inflammation, strengthening the association between allergic rhinitis and sinusitis. The mechanism of this inflammatory response needs to be elucidated.
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Raza, Fahad, Susanna Babasyan, Elisabeth M. Larson, Heather S. Freer, Christiane L. Schnabel, and Bettina Wagner. "Peripheral blood basophils are the main source for early interleukin-4 secretion upon in vitro stimulation with Culicoides allergen in allergic horses." PLOS ONE 16, no. 5 (May 26, 2021): e0252243. http://dx.doi.org/10.1371/journal.pone.0252243.
Full textAbstract:
Interleukin-4 (IL-4) is a key cytokine secreted by type 2 T helper (Th2) cells that orchestrates immune responses during allergic reactions. Human and mouse studies additionally suggest that basophils have a unique role in the regulation of allergic diseases by providing initial IL-4 to drive T cell development towards the Th2 phenotype. Equine Culicoides hypersensitivity (CH) is a seasonal immunoglobulin E (IgE)-mediated allergic dermatitis in horses in response to salivary allergens from Culicoides (Cul) midges. Here, we analyzed IL-4 production in peripheral blood mononuclear cells (PBMC) of CH affected (n = 8) and healthy horses (n = 8) living together in an environment with natural Cul exposure. During Cul exposure when allergic horses had clinical allergy, IL-4 secretion from PBMC after stimulation with Cul extract was similar between healthy and CH affected horses. In contrast, allergic horses had higher IL-4 secretion from PBMC than healthy horses during months without allergen exposure. In addition, allergic horses had increased percentages of IL-4+ cells after Cul stimulation compared to healthy horses, while both groups had similar percentages of IL-4+ cells following IgE crosslinking. The IL-4+ cells were subsequently characterized using different cell surface markers as basophils, while very few allergen-specific CD4+ cells were detected in PBMC after Cul extract stimulation. Similarly, IgE crosslinking by anti-IgE triggered basophils to produce IL-4 in all horses. PMA/ionomycin consistently induced high percentages of IL-4+ Th2 cells in both groups confirming that T cells of all horses studied were capable of IL-4 production. In conclusion, peripheral blood basophils produced high amounts of IL-4 in allergic horses after stimulation with Cul allergens, and allergic horses also maintained higher basophil percentages throughout the year than healthy horses. These new findings suggest that peripheral blood basophils may play a yet underestimated role in innate IL-4 production upon allergen activation in horses with CH. Basophil-derived IL-4 might be a crucial early signal for immune induction, modulating of immune responses towards Th2 immunity and IgE production.
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Choudhary, Shazia, Mamoona Noreen, Muhammad Arshad, and Muhammad Arshad. "Pollen Allergy; Mechanism and Etiology." NUST Journal of Natural Sciences 1, no. 1 (February 7, 2021): 16–19. http://dx.doi.org/10.53992/njns.v1i1.26.
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The term allergy refers to an exaggerated immune response to a foreign molecule. In a normal healthy individual, this foreign molecule will act as a harmless antigen, as it will be recognized & cleared by the immune system without causing any significant damage to host tissues. In certain individuals, such antigens stimulate immune system in such a way that a series of exaggerated immune response are generated against it, leading to significant tissue injury and damage to the host. Such as exaggerated immune response may also cause death of the patient. Such antigen is termed as an allergen. Allergy is categorised under Immunoglobulin E (IgE) mediated type I hypersensitivity reactions. These reactions occur when an antigen acting as an allergen attacks the immune system of the host and causes excessive stimulation of mast cells and basophils. This is followed by the release of allergy mediators which are responsible for causing local or systemic anaphylaxis, allergic asthma, allergic rhinitis, conjuctivitis. Type I allergens are of various types, the mechanism of action is same; however underlying factors may differ in each type. This article is about pollen allergens, in specific & will discuss the common sources of pollen allergens in Pakistan, the relevance and the factors behind pollen allergy.
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Nam, Joo Hyun, and Woo Kyung Kim. "The Role of TRP Channels in Allergic Inflammation and its Clinical Relevance." Current Medicinal Chemistry 27, no. 9 (March 27, 2020): 1446–68. http://dx.doi.org/10.2174/0929867326666181126113015.
Full textAbstract:
Allergy refers to an abnormal adaptive immune response to non-infectious environmental substances (allergen) that can induce various diseases such as asthma, atopic dermatitis, and allergic rhinitis. In this allergic inflammation, various immune cells, such as B cells, T cells, and mast cells, are involved and undergo complex interactions that cause a variety of pathophysiological conditions. In immune cells, calcium ions play a crucial role in controlling intracellular Ca2+ signaling pathways. Cations, such as Na+, indirectly modulate the calcium signal generation by regulating cell membrane potential. This intracellular Ca2+ signaling is mediated by various cation channels; among them, the Transient Receptor Potential (TRP) family is present in almost all immune cell types, and each channel has a unique function in regulating Ca2+ signals. In this review, we focus on the role of TRP ion channels in allergic inflammatory responses in T cells and mast cells. In addition, the TRP ion channels, which are attracting attention in clinical practice in relation to allergic diseases, and the current status of the development of therapeutic agents that target TRP channels are discussed.
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Rybachok, Oksana. "July 8, 2020 — World Allergy Day." Spravočnik vrača obŝej praktiki (Journal of Family Medicine), no. 7 (July 1, 2020): 69–73. http://dx.doi.org/10.33920/med-10-2007-10.
Full textAbstract:
Decision to celebrate World Allergy Day was adopted in 2005 at the initiative of the World Allergy Organization. The purpose of the initiative is to inform the general public about the symptoms of allergic manifestations, to promote regular inspections and examinations. One third of the adult population of the Russian Federation and one fourth of children and adolescents periodically suffer from manifestations caused by allergies. This disease is an immunopathological response of the body to the action of an agent as a result of the development of sensitization to it. Currently, there is a tendency to a steady increase in the manifestations of allergic responses, scientists attribute this to the increasing use of various preservatives, chemicals, dyes, new drugs, and cosmetics in everyday life. The main symptoms and manifestations of allergies include runny nose, red eyes, lacrimation, wheezing, bronchospasm, shortness of breath, various skin rashes, and headache can sometimes appear. One of the most dangerous manifestations of allergy is anaphylactic shock, which manifests itself in the form of itching, severe respiratory failure, profuse sweating, thready pulse, and a drop in blood pressure. This condition can be fatal if medical assistance is not provided on time.
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Skoner, David P., William J. Doyle, Sharon Boehm, and Philip Fireman. "Late Phase Eustachian Tube and Nasal Allergic Responses Associated with Inflammatory Mediator Elaboration." American Journal of Rhinology 2, no. 4 (September 1988): 155–61. http://dx.doi.org/10.2500/105065888781692998.
Full textAbstract:
Previous work in our laboratories has documented an IgE-mediated functional obstruction of the nose and eustachian tube (ET) immediately after nasal allergen challenge. The goals of this study were to monitor changes in nasal, ET, and bronchial physiology during the 12 hours following nasal allergen challenge and to correlate these changes with the elaboration of inflammatory mediators (IM). Subjects with ragweed allergic rhinitis were challenged intranasally with 2.5 mg of ragweed/nostril, and responses were assessed by posterior rhinomanometry for the nasal airway, sonotubometry for the eustachian tube, and spirometry for the bronchial airway. Blood was obtained simultaneously for quantitating the elaboration of three functionally and metabolically distinct IM. Late nasal responses (3–12 hours postchallenge) were observed in 7 of 10 subjects, with an average decrease of 67 ± 5% in nasal conductance at an average onset time of 6.6 ± 0.8 hours postchallenge. Dual late nasal responses were observed in five subjects. Late ET responses were observed in 10 ears (50%). Two sequential late ET responses were observed in three subjects. Late bronchial responses were detected in three subjects, one of whom did not have an early response. Plasma elevations of one or more IM were detected in all late nasal responders during the late phase response period. Late nasal and ET responses in association with an allergic nasopharyngeal inflammatory process could provide an important insight into the relationship between nasal allergy and middle ear disease.
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Wang, Yui-Hsi. "Developing food allergy: a potential immunologic pathway linking skin barrier to gut." F1000Research 5 (November 10, 2016): 2660. http://dx.doi.org/10.12688/f1000research.9497.1.
Full textAbstract:
Immunoglobulin E (IgE)-mediated food allergy is an adverse reaction to foods and is driven by uncontrolled type-2 immune responses. Current knowledge cannot explain why only some individuals among those with food allergy are prone to develop life-threatening anaphylaxis. It is increasingly evident that the immunologic mechanisms involved in developing IgE-mediated food allergy are far more complex than allergic sensitization. Clinical observations suggest that patients who develop severe allergic reactions to food are often sensitized through the skin in early infancy. Environmental insults trigger epidermal thymic stromal lymphopoietin and interleukin-33 (IL-33) production, which endows dendritic cells with the ability to induce CD4+TH2 cell-mediated allergic inflammation. Intestinal IL-25 propagates the allergic immune response by enhancing collaborative interactions between resident type-2 innate lymphoid cells and CD4+TH2 cells expanded by ingested antigens in the gastrointestinal tract. IL-4 signaling provided by CD4+TH2 cells induces emigrated mast cell progenitors to become multi-functional IL-9-producing mucosal mast cells, which then expand greatly after repeated food ingestions. Inflammatory cytokine IL-33 promotes the function and maturation of IL-9-producing mucosal mast cells, which amplify intestinal mastocytosis, resulting in increased clinical reactivity to ingested food allergens. These findings provide the plausible view that the combinatorial signals from atopic status, dietary allergen ingestions, and inflammatory cues may govern the perpetuation of allergic reactions from the skin to the gut and promote susceptibility to life-threatening anaphylaxis. Future in-depth studies of the molecular and cellular factors composing these stepwise pathways may facilitate the discovery of biomarkers and therapeutic targets for diagnosing, preventing, and treating food allergy.