Thesis--Copenhagen. / "Translated from Danish by Mrs. Clara Packness." "Résumé" (in Danish): p. [215]-222. Bibliography: p. [223]-229.

Thesis (M.A.) -- Central Connecticut State University, 2006. / Thesis advisor: Marc Goldstein. "... in partial fulfillment of the requirements for the degree of Master of Arts in Psychology." Includes bibliographical references (leaves 42-45). Also available via the World Wide Web.

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This thesis describes the procedures used in preparation of the derivatives of certain alkyl phenylacetates and the necessary intermediate compounds. Compounds resembling the structure of Benadryl were prepared in this study in the hope that at least one might prove to be of value in the fight against allergy.

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Exposure to sufficiently high allergen levels of some allergens appears to protect against the development of allergic diseases, and has also been used to treat established allergic diseases. A reduced prevalence of sensitization and, in some cases, asthma was reported among individuals living in homes with high allergen levels. Furthermore, allergic patients treated with high allergen doses during immunotherapy experienced improved allergic symptoms. The mechanisms for how high allergen exposure may prevent disease are not known and thus, a model in which these mechanisms could be studied in detail is warranted. The objective of this thesis was to model and further characterize the phenomenon of high allergen dose-dependent protection against the development of allergic responses, using a mouse model of epicutaneous sensitization. The impact of exposure to a high dose of cat dander in established allergic disease was also evaluated. Epicutaneous exposure to a high dose of cat dander (150 μg) prevented airway inflammation and airway hyperresponsiveness in genetically different strains of mice, including Th2 prone BALB/c mice. The protective effects against airway inflammation appeared to wane between 10 and 120 days after exposure. When the high dose of cat dander was applied with a sensitizing dose of peanut, peanut induced anaphylaxis was prevented. Exposure to a high dose of another allergen, ovalbumin, was also able to prevent the development of allergic airway disease. In contrast, the high dose of cat dander did not improve established states of allergic disease. Thus, in our mouse model, a high dose of cat dander prevented the development of allergic responses and reflected characteristics of the phenomenon reported in humans. As such, this model may be useful for investigating mechanisms and potential prophylactic options for allergic diseases. As the high dose of cat dander either had no effect or worsened established allergic responses in our model, it is possible that the dose was not high enough to improve disease in sensitized mice. It is also possible that established disease cannot be modified by epicutaneous exposure. / Thesis / Master of Science (MSc)

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The role of T and B lymphocytes in the human immune response has been studied in allergic and asthmatic patients by many investigators. Theories of suppressed cellular immunity have been reported showing decreased levels of T cells in peripheral blood. Elevated levels of IgE, an antibody, have been reported in these conditions, but not shown to be significant in distinguishing the different types of asthma. A double blind study of 19 allergic and 42 asthmatic individuals was conducted measuring T and B cell levels and IgE levels. The asthmatic group was subdivided into three types, intrinsic, extrinsic and mixed. The possible effects of corticosteroids were considered with each group since 47 out of the total 60 patients studied were steroid dependent. T and B cells were enumerated by rosette method. This method was developed and normal values established. IgE levels measured by radioimmunoassay. Results showed all steroid dependent patients, allergic and asthmatic, had normal or slightly elevated T and/or B cell levels and IgE levels. The corticosteroids appeared to have a simulative effects rather than a suppressive effect on T and B cells and IgE as previous investigators have reported. Allergic or asthmatic conditions cannot be distinguished on the basis of T and B cell levels. IgE levels were found to be highly significant at a 95% confidence level in distinguishing intrinsic asthma from extrinsic asthma.

The early phase of allergic reactions is largely dominated by IgE-mediated degranulation of mast cells and basophils. Mast cells and basophils release mediators which include histamine, prostaglandins, leukotrienes, cytokines, etc. Histamine is a biogenic compound that can directly cause physiological changes that ultimately contribute to allergy and asthma symptoms. The current literature focused on the study of histamine production from “professional histamine producers”, such as mast cells and basophils in allergic diseases. Previous research had shown that activation of allergic specific T cells led to airway narrowing independent of basophil activation 6-hour post exposure. It was therefore possible that the activation of T cells may release histamine which contributed to the airway narrowing observed. This project aimed to determine expression of histidine decarboxylase (HDC) in T lymphocytes, which is the gene encoding the enzyme solely responsible for the production of histamine. We found that HDC is expressed in rare T cell populations by the bioinformatic analysis of publicly available datasets, and we found that the activation of human primary CD4+ T cells by anti-CD3/CD28 did not lead to the upregulation of HDC by qPCR. The activation of CD4+ T cells in non-allergic donors led to a LOG2FC of HDC to B2M housekeeping gene of: -1.0 +/- 0.48 at 6-hour, -1.3 +/- 0.23 at 24-hour, -2.2 +/- 0.32 at 72-hour. The activation of CD4+ T cells in allergic donors led to a LOG2FC of HDC of: -0.48 +/- 0.13 at 6-hour, -2.1 +/- 0.35 at 24-hour, -4.1 +/- 1.1 at 72-hour. In conclusion, HDC expressing T cells were rare and of low expression level. The activation of CD4+ T cells did not upregulate HDC and therefore it was unlikely that T cell derived histamine contribute to allergic manifestations. / Thesis / Master of Science in Medical Sciences (MSMS)

Abstract not available