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Orientador: Paulo Inácio da Costa / Banca: Virginia Paes Leme Ferriani / Banca: Cleni Mara Marzocchi Machado / Resumo: A alergia à proteína do leite de vaca (APLV) é comum no primeiro ano de vida e o seu reconhecimento e diagnóstico são difíceis. A proposta deste estudo é verificar a expressão de fenótipos linfocitários, as citocinas padrão Th1 e Th2, e a IgE total e específica em crianças com APLV, crianças atópicas (AC) e não atópicas (NAC) e suas respectivas mães.Foram colhidas amostras de sangue periférico para tipagem de linfócitos por citometria de fluxo, e dosadas as citocinas séricas, por CBA (Cytometric Bead Array) e dosado a IgE total e específica para as proteínas caseína, α lactoalbumina e β lactoglobulina , das crianças e suas mães nos grupos APLV, AC e NAC.Nas crianças do grupo APLV o início dos sintomas foi por volta dos 5,1 meses de idade, com idade média de 17,25 meses (sd=14,8 meses). As crianças e suas mães dos grupos alérgicos (APLV e AC) mostraram maior número de linfócitos CD4+CD25+ (p<0,05) em relação àquelas do grupo não alérgico (NAC), mas sem diferença significativa (p>0,05) entre os grupos APLV e AC. O grupo APLV mostrou maior tendência à presença do fenótipo CD25. As concentrações séricas das citocinas IL4, IL5, IL10, IL2, TNF-α e IFN-γ, entre os grupos estudados, não apresentaram diferenças estatísticas significantes (p>0,05), porém houve uma maior tendência à expressão da IL10 nas crianças do grupo APLV. A IgE total ficou mais evidente no grupo APLV do que nos demais grupos, e os principais alérgenos foram a α-lactoalbumina e β lactoglobulina. As crianças com alergia ao leite de vaca apresentam uma maior positividade de linfócitos CD4+CD25+, presença de IgE total e expressão de IL10 in vivo o que também pode sugerir um meio de controle da alergia para desenvolver tolerância à proteína do leite de vaca... (Resumo completo, clicar acesso eletrônico abaixo) / Abstract: The allergy to cow‟s milk protein (CMA) is common in the first year of life and it is difficult to acknowledge and diagnose it. This study aims to verify the expression of lymphocyte phenotypes, detect the TH2 and TH1 pattern cytokines and the total and specific IgE in CMA children, in atopic (AC) and non-atopic (NAC) children and their respective mothers. Samples of peripheral blood were collected in order to type the lymphocytes by flow cytometry, dosed the serial cytokines by Cytometric Bead Array (CBA) and dosed the total IgE and specific IgE for the casein, α lactoalbumin and β lactoglobulin proteins of the children and their mothers in the CMA, AC and NAC groups. In the CMA children the symptoms first occurred around 5,1months old, with the average age of 17.25 months (sd=14.8 months). The children and their mothers from the allergic group (CMA and AC) showed significantly presence of CD4+CD25+ lymphocytes (p<0.05) higher than the non-allergic group (NAC), but without any significant difference (p>0.05) between the CMA and AC groups, although there was a tendency to an increase presence of these cells in the CMA group. The serial concentration of the IL4, IL5, IL10, IL2, TNF-α and IFN-γ cytokines, among the studied groups, did not present significant statistical difference (p>0.05), however, there was a tendency to an increase expression of IL10 in the CMA group of children. The total IgE was more evident in the CMA group than in the other ones and the main proteins which caused allergic reactions were α-lactoalbumin e β lactoglobulin. The children with cow‟s milk allergy presented a higher positivity of CD4+CD25+ lymphocytes, higher total IgE and an increase expression of in vivo IL10, which may also suggest a means of control of the allergy to develop tolerance to the cow‟s milk proteins... (Complete abstract click electronic access below) / Mestre

Thesis (M.A.) -- University of Texas at Arlington, 2008.

Once thought to be an uncommon disease, the number of cases of Eosinophilic Esophagitis (EoE) are rapidly increasing, affecting patients across the age, gender, and ethnic spectrum. EoE is an allergy-induced disease process that affects the cellular makeup of the esophagus, which in turn causes inflammation and fibrosis within the esophagus. EoE can cause chest pain, dysphagia, food bolus impaction, and a failure to thrive (FTT) in adolescents. EoE is currently treated with diet modification, and by swallowing topical corticosteroids. Advanced EoE, may result in esophageal remodeling that requires physical intervention, in order to maintain swallowing functionality. New drug therapies and genetic research are being explored, in the search to find treatments that address both the symptomology and histology of EoE.

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This thesis presents a sociological framework for understanding food allergy. Food allergy is increasingly appearing on policy and media platforms in contemporary Western societies. Debates have emerged about the prevalence of food allergy and also about the “rights” of those experiencing food allergies in a number of public and private spheres. Food allergy is a specifically social phenomenon, emerging as a consequence of modernization processes. Additionally, the allergy “zone” is comprised of a number of actors and agents including the institutions of medicine, pharmaceutical companies, politicians, governments, lay actors and an array of medical technologies. Despite being an issue of major sociological significance, few empirical studies have explored the everyday experience of food allergy. Therefore, in order to understand the lived experience of food allergy, I construct a conceptual framework which draws upon theories of risk and social governance, the sociology of consumption and sociological studies of science and embodiment. These literatures shed important light upon how individuals negotiate and (de)construct the risks associated with their conditions. Drawing on data acquired from eight in-depth interviews with those who identify as food allergic, I argue food allergy need be understood as a form and practice of consumption. Thus, far from being passive subjects, this approach characterises individuals as being embodied and reflexive agents who actively deconstruct notions of risk and recurrently engage in practices of “edgework”. These actors negotiate the medical and scientific parameters of their conditions as well as the parameters and demands of consumer culture. Whilst these theoretical and conceptual frameworks are useful for understanding the experience of food allergy, I recommend further studies of food allergy acknowledge the diversity of actors/institutions involved in the discursive production and circulation of information about food allergy; specifically homeopathic and alternative practitioners and organizations. Additionally, I argue that future studies of allergy must acknowledge the fundamentally embodied experience of the condition and the consequences this has for its definition and experience. For the purposes of future studies of food allergy, I also suggest it would be worthwhile to further explore the ways in which individuals who experience food allergies and intolerances are enrolled and participate in biopolitical regimes. / Thesis (Master, Sociology) -- Queen's University, 2011-09-14 14:03:42.479

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The study mainly focuses on the role of dendritic cells (DCs)，especially DC subsets, in modulating intracellular bacterial infections and the modulating effect of these infections on allergic responses. Specifically, it investigated the molecular mechanisms of 1) mycobacterial infection, 2) chlamydia infection and 3) the effect of these infections on allergic reactions. The results demonstrated that Bacillus Calmette-Guérin (BCG) vaccination promoted the expansion of CD8+DCs, which showed a more mature phenotype and produced more IL-12 compared to CD8-DCs. In vivo BCG-primed CD8+DC, but not CD8-DC, was the dominant DC subset in inducing protective immunity against BCG infection. Further, the results showed that adoptive transfer of different DC subsets from BCG-infected mice inhibited OVA-induced allergic reactions through immune deviation and immune regulation mechanisms. In addition, the results showed that CD8+DCs primed by Chlamydia, another intracellular bacterial pathogen, inhibited the allergic responses through IL-10 dependent pathway. Further, the data demonstrated that IL-10 inhibited the expansion of protective Th17 cells following Chlamydia infection. DCs from IL-10 KO mice showed significantly higher ICOS ligand (ICOS-L) expression compared to WT mice. Th17 from Chlamydia infected mice, but not Th1 cells, expressed high levels of ICOS. Blockade of ICOS/ICOSL signaling virtually abolished the Th17 promoting effect of DCs from IL-10 KO mice but had no significant effect on Th1 cells. This study provided new knowledge on the immune regulation of DC, especially its subsets, which may be helpful for the rational development of new preventive or therapeutic methods to tuberculosis / Chlamydia infections and allergic diseases.