The mechanism and physiology of nasal allergy were studied by means of techniques such as histochemistry, biochemistry, immunochemistry, autoradiography, vital microscopy and electronmicroscopy etc. The conclusions were as follows. 1. When allergic particle attached and deposited on the surface of the nasal mucous membrane, antigen was dissolved in the mucous blanket and penetrated into the epithelial layer. During the process reagenic or precipitate antibodies contained in the blanket were against the penetration of the antigen. 2. Immediately after antigen entered into the epithelial layer, antigen-antibody reaction occured possibly on the surface of the epithelial cells, being followed by the damage of the cells. The damage developed to manifestation of nasal symptoms such as sneezing, watery discharg and nasal obstruction. 3. There were many evidences, in which chemical mediator was not responsible for the first stage of the nasal allergic reaction in the epithelial layer. 4. The allergic reaction had to be appreciated as a defence mechanism against the penetration of foreign body into the mucous membrane. Sneezing reflex expelled an allergen from the surface of the membrane, and profuse watery secretion which came from the secretory gland and goblet cell washed out the surface. Nasal obstruction prevented any more penetration of the allergen into the nasal cavity. 5. Allergic reaction was influenced by the degree of the sensitization and sensitivity of the membrane. Local vagotonia caused an increase in the hydrogen ion concentration and decrease in the viscosity of the mucous blanket. Those accerelated the absorption rate of the antigen in the mucous membrane. 6. There were a local disturbance of the condition of the vasomotor nerve in vasomotor rhinitis which had nasal allergy like syptomes whithout negative skin test, although it was lesser than in nasal allergy. It was also shown that the occurrence of vasomotor rhinitis needed some other than vasomotor disturbance. 7. By specific hyposensitization with allergen extract improvement of symptome, decrease of watery discharge, eosinophilia, reaction in provocation and skin test with allergen were obtained in many caces of nasal allergy. In the improved cases there was an appearance of heamagglutination antibody in the blanket, using the bis-diazotized-benzidin technique, and decrease in the sensitivity of the epithel cell to offending allergen.

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Inhibitory effects of chemical mediator liberation following an antigen-antibody reaction were reported on inhaled Intal. To investigate further efficacy on this drug on children in asthma, influences on 1) provocative inhalation with extract of house dust, 2) on airway histamine hypersensitivity, 3) on daily pulmonary function, were studied. Pretreatment by the inhalation of the Intal resulted in complete inhibition of asthmatic reaction to bronchial provocative test with H.D. in 2 cases and also resulted in significant elevation of H.D. threshhold in 6 of 7 cases. Elevation of histamine threshhold over 25% to control value was found in about 60% of 29 pretreated tests with the Intal. Two of influenced cases showed no meaningful reduction in PEFR measurements even after the inhaltion of 500 γ of aerosole histamine. In four times daily PEFR measurement statistically significant improvemant in pulmonary function produced by 3 times daily Intal inhalation was found in 60% of 13 trials, which was consisted of 5 days of Intal administration and every 5 days for control both before and after Intal period. These observations indicate that the Intal not only interfers with the liberation of chemical mediators following an antigen-antibody reaction but also reduces itself the airway histamine hypersensitivity and bronchospasm characteristic to asthmatic patents.

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The chemical mediator of a cold urticaria patient was examined. This wheal was not prevented by diphenhydramine (an antihistamine) or aprotinin (Trasylol, an antikallikrein agent), and decreased after the recurrent cold stimuli or the injection of sinomenine (a mast cell degranulating agent). Histamine was not demonstrated in the skin of the patient by the dermal perfusion technique when ice was applied. The dermal perfusion technique consists of a delivery and a collecting needle inserted superficially 0.5 cm apart into the dorsal skin of the forearm, with sterile isotonic saline entering the skin at the delivery site, perfusing the dermal-subcutaneous tissue, and via the collecting needle. The dermal perfusate was examined by a rabbit vein bioassay. Kinin activity was present in the dermal perfusate. 5-HT or histamine was not found in the perfusate by the thin layer chromatography technique. The increasing of plasminogen activator activity and plasmin activity by application of ice was not found. In this case, it may be possible to explain the localized and systemic reactions of cold urticaria by kinin effect since kinins were found in the persusion fluid of the wheal induced by cold. The kinin forming enzyme activity of the mast cells may increase by application of cold, and these may split plasma proteins to produce kinins.

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Air-borne fungus was investigated by using subouroud medium exposed 15 minutes or 2 hours in the patient room. Ten species of fungi were detected; i.e. Aspergillus, Penicillium, Alternaria, Fusarium, Carvararia, Neurospora, Trichoderma, Paecilomyces, Cephalosporium and Acrostalagums. Colony-counting in the exposed medium was markedly increased in summer and clear weather, however there was no difference in colony-counting between patients houses and patient room in the hospital. Positive rates of skintest for five fungus antigens were markedly high in the asthmatic patients as 65% of Candida, 30% of Penicillium and about 20% of other three antigens. Threshold value in the patient skintest as well as PK test was markedly high as 160,000×in 84% of all patients. The hyposensitization test by fungus antigen was successful in 18 cases of 26 cases. In 14 improved cases, blocking antibody was markedly recognized. The hyposensitization by house dust antigen influenced to the decrease of sensitivity to the fungus antigen. Furthermore, hyposensitization by both of house dust and fungus antigen were effective to the decrease of both sensitivity.

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It has been known that the cellular immunity which produces the delayed type allergy, may render the resistance to some bacterial infections such as tuberculosis, salmonellosis, listeriosis, and so on. In viral infections it has also been indicated that the cellular immunity besides the humoral antibody may possibly show resistance to infection by various clinical observations. Onto the above findings, the present investigation was made by use of Ectromelia virus (Hamptead strain)(EV)-mice system in order to study whether the cellular immunity reveals the resistance to the viral infection. The Cowpox virus (LB red strain) and EV were vaccinated to mice by the method of Kato et al. (1966). The cells from the peritoneal exudates and the spleen of the vaccinated animals were injected into the normal mice intraperitoneally. Then, it was observed that the non-treated mouse was dead in between six to nine days, while it was seen that any mouse treated with vacicnated cells was scarcely dead. However, the mice that were transferred with cells from immunized peritoneal exudates and spleens which were damaged by freezing and thowing, the small amount of the anti EV immune sera, the supernatant of immune peritoneal exudate and cells from non-immunized peritoenal exudates and spleens, showed high mortality by EV challenge, respectively. It was assumed by the above results that the cellular immunity has the resistance to infectious death in EV-mice system.

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