There is increasing interest in the role played by the cysteinyl leukotrienes in the pathogenesis of bronchial asthma. They have been demonstrated to have a bronchoconstrictor effect both in vitro and in vivo and have been isolated from bronchoalveolar lavage fluid and urine from stable asthmatics and from asthmatics during exacerbations and after endobronchial challenge. Pharmacological intervention has been studied through antagonism of leukotriene receptors and inhibition of leukotriene synthesis. Both have been shown to have an effect on the asthmatic response after challenge with allergen, exercise and inhalation of cold air and to have an effect on aspirin sensitive asthmatics and on the symptoms and markers of severity of chronic asthma. The differences between receptor antagonism and synthesis inhibition are discussed.

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Urticaria occurs commonly in children and young adults. In general, a younger and atopic population is usually involved and the lesions are acute, usually less than 6 weeks in duration and it is relatively easy to show a cause and effect, usually by history. The cause of chronic urticaria, which is defined as urticaria lasting longer than 6 weeks, is much more difficult to identify and 80-95% of patients are classified as idiopathic. Many of the patients react with a wheal and flare to their own serum or plasma indicating that they have a histamine-releasing agent in their own serum. Most of these subjects will have urticaria which clears with time but a small minority continue to have urticaria for the rest of their lives.
Treatment for patients having known causes is to avoid the triggers and all patients with chronic urticaria need to be treated with H1 antihistamines. Sometimes an H2 antihistamine is added or a tricyclic ‘tranquilizer’ which has anti H1 and H2 blocking action needs to be used. Those patients who do not respond may need treatment with prednisone which should be reduced to the smallest dosage and discontinued as soon as possible. Patients with hereditary angioedema respond to danazol, stanozol or epislanaminocaproic acid or tranexamic acid.

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Expression of antigen-specific serum IgE and IgA, and saliva IgA were measured in four volunteers using a Multiple Antigen Simultaneous Test (MAST). Two donors, expressing allergen-specific IgE in serum, expressed antigen-specific serum IgA strongly, but saliva IgA weakly. The other two donors, not expressing serum IgE, expressed serum IgA weakly and saliva IgA strongly. These results suggest a possibility that secretory IgA plays an important role in the prevention of food allergy. To clarify the role of IgA, further investigation on allergic patients is necessary.

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The polypeptides in Hinoki cypress (Chamaecyparis obtusa) and Japanese cedar (Cryptomeria japonica) extracts were analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), and then IgE binding activities were examined by immunoblotting using sera from 25 patients with Japanese cedar pollinosis. Fifteen component bands with IgE binding abilities were detected. The most frequent IgE binding band was observed on the line of 45kDa (92%), followed by 50 (88%) and 74kDa (52%). The immunoblotting profile of Hinoki cypress was different from that of Japanese cedar. In the inhibition immunoblotting test, IgE binding activities of 14, 30-35 and 74-85kDa components in Japanese cedar extract and 14, 30-35 and 60-74kDa proteins in Hinoki cypress extract were completely inhibited with heterologous extracts. However, those of the 41kDa proteins and 46kDa in Japanese cedar extract and 45 and 50kDa components in Hinoki cypress extract were partially inhibited. These data suggest that 45 and 50kDa components of Hinoki cypress and 41 and 46kDa components of Japanese cedar share some cross-reacting and specific epitopes.

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The cytokine network plays an important role in the pathogenesis of allergic asthmatic lung. As the influence of smoking on cytokine expression should be considered in delineating the cytokine network, the effects of a single exposure and chronic exposure to smoke on the number and cytokine expression of bronchoalveolar lavage fluid (BALF) cells were evaluated. From a total of 126 BALB/c mice, BALF cells were obtained and analyzed using the quantitative reverse transcription-polymerase chain reaction technique (RT-PCR).
The bodyweights of chronic smoking mice were found to be lower when compared to those mice that had not been exposed to smoke. The total number of BALF cells increased after smoking without significant differences in cell classification. Spontaneous mRNA expression of interleukin-1α (IL-1α), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and transforming growth factor-β (TGF-β) was detected in all cases. The time courses of their expression patterns after exposure to smoke were similar between the chronic and single smoking mice, except for TGF-β. The levels of IL-1α, IL-1β and TGF-β mRNA increased immediately after the exposure to smoke in chronic smoking mice, whereas the levels of TGF-β mRNA increased 2h after exposure in the single smoking mice. Moreover, the increase of IL-1α and TGF-1β mRNA in the early phase after exposure was exaggerated in chronic smoking mice.
Thus, repeated exposure to smoke may have caused some alterations in the expression mechanism of cytokines such as TGF-β and IL-1α in BALF cells, while it seemed to cause a repeated pattern of acute inflammation after each exposure. In the evaluation of cytokine expression in BALF cells in smokers with various lung diseases, it is recommended that before taking samples a sufficient time interval after the last exposure to smoke be allowed to avoid the effect of acute inflammation caused by smoking.

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Sera from 27 patients with mite-sensitive allergic rhinitis, without atopic dermatitis and bronchial asthma, were examined for anti-Der f I and anti-Der f II IgE antibody contents by enzyme-linked immunosorbent assay (ELISA). Anti-Der f I and anti-Der f II IgE antibody levels were 14.78±1.34 and 32.68±0.88ng/mL (mean±SEM), respectively. The anti-Der f II IgE antibody was predominant over the anti-Der f I IgE antibody in these patients.
In comparison with the results of a previous study the present study indicates that the ratio between serum anti-Der f I and II IgE antibodies in patients with allergic rhinitis indicated the same pattern as in that of patients with bronchial asthma, while the inverse was the case in patients with atopic dermatitis.
These results indicate that immunological features and major allergen molecules could be different in different atopic diseases. At present it is not clear where this difference comes from, but the route of immunological sensitization (via respiratory tract vs via skin) might result in the difference.

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The role played by the interaction of nitric oxide (NO) and endothelins (ET) in the modulation of airway function, and the modulation of β-adrenergic-mediated bronchodilator responses by ascorbic acid in the presence or absence of endogenous NO induced by ET in anesthetized guinea-pigs was examined. Endothelins induced a concentration-dependent increase in respiratory resistance, and pretreatment with the NO synthase inhibitor, N_G-nitro-L-arginine methylester, (L-NAME), significantly increased ET-mediated bronchoconstriction. In addition, ET-3-mediated bronchoconstriction following pretreatment with L-NAME was reversed by L-arginine. These findings suggest that the response to the administration of ET-3 can be attributed to the release of NO from the guinea-pig airway. Neither inhaled isoproterenol nor salbutamol significantly affected ET-3-mediated bronchoconstriction, but pretreatment with L-NAME markedly enhanced isoproterenol-mediated bronchodilatation. These findings suggest that endogenous NO induced by ET-3 may attenuate isoproterenol-mediated bronchodilator responses. Ascorbic acid, an antioxidant, enhanced isoproterenol-mediated bronchodilator responses following pre-contraction with ET-3, but pretreatment with L-NAME reduced this effect of ascorbic acid. The findings suggest that ascorbic acid attenuates the effect of endogenous NO on β-adrenergic-mediated bronchodilator response via its antioxidant activity. Since 10^-7mol/L ET-1 does not induce the release of NO from the guinea-pig airway, ascorbic acid cannot enhance isoproterenol-mediated bronchodilator responses. It seems likely that endogenous NO plays an important regulatory role in modulating β-adrenergic-mediated bronchodilator responses in the airway.

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Aspergillus restrictus, an osmophilic fungus, is abundant in house dust. We have shown previously that the incidence of immediate hypersensitivity to A. restrictus is comparable to that for Aspergillus fumigatus and Alternaria alternata in asthmatic children. Radioallergosorbent test (RAST) inhibition was used to determine whether A. restrictus shares similar allergenic components with A. fumigatus and A. alternata. Mycelial mats of the three species cultivated on completely synthetic media were used for extract preparation. IgE antibodies to each fungus were measured with RAST using a polyvinyl chloride microplate as a solid phase. Analysis of a serum pool obtained from nine asthmatic children with a positive RAST to A. restrictus showed that A. restrictus inhibited the RAST to A. restrictus, A. fumigatus and A. alternata by more than 80%. Similar results were observed with A. fumigatus and A. alternata. Additionally, when 13 serum samples with a positive RAST to A. restrictus were tested separately, A. restrictus substantially inhibited the A. restrictus RAST in all subjects tested. A. fumigatus and A. alternata inhibited the A. restrictus RAST in 10 and 8 of the samples studied, respectively. These findings indicate that A. restrictus shares allergenic components with A. fumigatus and A. alternata. The allergenic cross-reactivity between A. fumigatus and A. alternata was also demonstrated.

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