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Rings of intrapulmonary bronchi isolated from rabbits producing anti-horseradish peroxidase IgE antibodies contracted when exposed to antigen. The contractile response had a lag period of about 1 min, reached a peak at 6 min and then subsided. Bronchi from rabbits with detectable levels of specific IgG (in addition to IgE) antibodies did not differ in response from those with undetectable specific IgG levels. Histamine also contracted rabbit intrapulmonary bronchi with an EC50 of 10ωM (SD 1.29). The response to antigen was completely inhibited with chlorpheniramine (30 ωM). In contrast to intrapulmonary bronchi, responsiveness of mainstem bronchi to antigen was observed only occasionally, whereas histamine was equipotent on both mainstem and intrapulmonary bronchi. Thus, the amount of antigen-induced mediator release may be less in the mainstem bronchi. Acetyl glyceryl ether phosphorylcholine, in concentrations up to 10 ωM, did not contract either mainstem or intrapulmonary bronchi. This study indicates that histamine is the major mediator of (and acetyl glyceryl ether phosphorylcholine does not significantly participate in) antigen-induced contraction of isolated bronchi from IgE-producing rabbits. The results provide a likely mechanism for the increase in pulmonary resistance observed in IgE anaphylaxis in this species.

The association between acute coronary events and acute allergic reactions has been recognized for several years. The first reported case occurred in 1950, during an allergic reaction to penicillin. In 1991, Kounis and Zavras described the syndrome of allergic angina and allergic myocardial infarction, currently known as Kounis syndrome. Two subtypes have been described: type I, which occurs in patients without predisposing factors for coronary artery disease and is caused by coronary artery spasm, and type II, which occurs in patients with angiographic evidence of coronary disease when the allergic events induce plaque erosion or rupture. This syndrome has been reported in association with a variety of medical conditions, environmental exposures, and medication exposures. Entities such as Takotsubo cardiomyopathy, drug-eluted stent thrombosis, and coronary allograft vasculopathy appear to be associated with this syndrome. In this review, we discuss the pathobiology, clinical features, associated entities, and management of Kounis syndrome.

Allergen-reactive CD4+ T cells are implicated in the pathogenesis of allergic disease. Peptide immunotherapy (PIT) involves therapeutic administration of short immunodominant peptides from within the protein allergen to which CD4+ T cell responses are directed. This approach can induce tolerance of allergen-reactive CD4+ T cells, while negating the risk of severe allergic reactions associated with whole allergen specific immunotherapy. PIT therefore holds promise as a diseasemodifying treatment for allergic patients. However, further information regarding the mechanisms of action of PIT are required to aid translation to the allergy clinic. Chicken ovalbumin (OVA) is a commonly used model allergen in mouse models of allergic airways inflammation (AAI). Trackable, T cell receptor transgenic T cells recognizing the immunodominant 323-339 peptide of OVA (pOVA) allow mechanistic investigation of PIT in response to pOVA. This thesis investigated the hypothesis that strong, systemic T cell responses induced by intravenous administration of soluble pOVA will induce i) tolerance to pOVA and ii) linked suppression to any additional OVA T cell epitopes, hence improving OVA-induced AAI. Contrary to the hypothesis, intravenous pOVA PIT did not improve disease in a C57BL/6 model of OVA-induced AAI. Models of OVA-induced allergic sensitisation and AAI were therefore developed incorporating trackable CD4+ pOVA-reactive T cells (OT-II cells). pOVA PIT induced tolerance of these cells in an allergic sensitisation setting, but had limited impact on the overall OVA response. Yet, in a model of AAI driven solely by Th2 polarised CD4+ OT-II cells, pOVA PIT did improve disease. It was concluded that, in non-transgenic C57BL/6 mice, CD4+ T cells responding to additional epitope(s) within OVA were important in driving disease and that these T cells were not subject to linked suppression following pOVA PIT. Using a panel of overlapping peptides constituting the sequence of OVA, a novel CD4+ epitope within OVA was characterised. The effects of PIT using pOVA in combination with a peptide containing this additional epitope on OVA-induced AAI were then assessed. Findings from this project therefore hold importance for future mechanistic work surrounding PIT in allergic disease.

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The purpose of this manuscript was to present a brief history, the current status, and a prospectus of allergen and allergic reactions. Research on allergic reactions, particularly as viewed from the psychogenic position, was presented. The review strongly suggests that the psychogenic orientation has been frought with contradictions, unnecessarily complex interpretations, and an over-abundance of subjective, dynamic, and analytic redundancies which have done little more than perpetuate the stagnation of a rather important subdomain of the "mental" health professions.