Allergology International (Allergol Int )

Publisher: Nihon Arerugī Gakkai


Allergology International is the official journal of the Japanese Society of Allergology and publishes original papers dealing with the etiology, diagnosis and treatment of allergic and related diseases. Papers may include the study of methods of controlling allergic reactions, human and animal models of hypersensitivity and other aspects of basic and applied clinical allergy in its broadest sense. The Journal aims to encourage the international exchange of results and encourages authors from all countries to submit papers in the following five categories: Original Articles, Case Reports, Short Communications, Occasional Reviews and Editorials, Letters to the Editor, and Hypothesis.

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    Allergology International website
  • Other titles
    Allergology international (Online), Allergol Int
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    Document, Periodical, Internet resource
  • Document type
    Internet Resource, Computer File, Journal / Magazine / Newspaper

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: Thrombomodulin treatment modulates the properties of dendritic cells (DCs) converting them from immunogenic to tolerogenic and inducing its own expression on DCs. Thrombomodulin binds to the inflammatory mediator, high mobility group protein B1 (HMGB1), antagonizing signalling through its receptor, receptor for advanced glycation end products (RAGE). Methods: To test if soluble thrombomodulin could antagonize HMGB1 signaling via RAGE on DCs. DCs were prepared from mouse bone marrow cells or human monocytes. In some experiments dendritic cells were sorted into thrombomodulin+ and thrombomodulin- populations. Expression of surface maturation markers was determined by flow cytometry following treatment with thrombomodulin in the presence or absence of HMGB1. Results: Thrombomodulin+ dendritic cells secrete less HMGB1 into the medium. HMGB1 reduces the effects of thrombomodulin on expression of DC maturation markers. Treatment with thrombomodulin reduces the expression of maturation markers such as CD80 and CD86 and increases the expression of thrombomodulin on the DC surface. Treatment of DCs with neutralizing anti-HMGB1 antibody acted synergistically with thrombomodulin in increasing thrombomodulin expression on DCs. Treatment with thrombomodulin can still reduce the expression of surface markers on DCs derived from mice that are deficient in RAGE showing that thrombomodulin can affect DCs by an alternative mechanism. Conclusions: The results of this study show that thrombomodulin modulates DCs both by antagonizing the interaction of HMGB1 with RAGE and by an independent mechanism.
    Allergology International 12/2013;
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    ABSTRACT: Basophils represent less than 1% of peripheral blood leukocytes. They are often recruited to the site of allergic inflammation, albeit in small numbers. However, it remained uncertain whether basophils play any significant role in allergic reactions or act as minor and redundant 'circulating mast cells'. We have recently demonstrated that basophils play critical roles in systemic anaphylaxis and chronic allergic inflammation, distinctively from mast cells. Basophils are one of the major players in the IgG- but not IgE-mediated systemic anaphylaxis, in contrast to mast cells. In response to the allergen-IgG immune complexes, basophils release the platelet-activating factor rather than histamine as the major chemical mediator to induce the systemic anaphylaxis. The depletion of basophils protects mice from death due to anaphylactic shock. Basophils also play a crucial role in the development of the IgE-mediated chronic allergic inflammation with massive eosinophil infiltration in the skin, independently of T cells and mast cells, even though basophils account for only approximately 2% of the infiltrates. The basophil depletion shows a therapeutic effect on on-going allergic inflammation. Accumulating evidence suggests that basophils function as initiators rather than effectors of the chronic allergic inflammation. Thus, basophils and their products seem to be promising therapeutic targets for allergic disorders.
    Allergology International 02/2009; 58(1):11-9.
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    ABSTRACT: We have recently found that exposure to acute restraint stress suppresses antigen-specific antibody production, including IgE, in a murine model of allergic rhinitis. Although age-related alterations in immune responses are known, it remains unclear whether aging modulates the antibody production under stressful conditions. In this study, we set out to determine the effects of aging on antibody production under acute restraint stress in mice. Both young and aged CBA/J mice were repeatedly sensitized intranasally with phospholipase A2 (PLA2) without adjuvants. Restraint stress was applied using uniform cylinders once a week for a continuous 8h period, on 5 occasions in total. Blood samples were taken at 0, 20 and 30 days after primary sensitization, and production of PLA2-specific antibodies and levels of IL-4, IFN-gamma, IL-10 and IL-1 beta in sera were determined by ELISA. Repeated intranasal sensitization with PLA2 induced PLA2-specific IgE, IgG1 and IgG2a production in aged mice. We found that exposure to restraint stress significantly inhibited production of PLA2-specific IgE, IgG1 and IgG2a in aged mice. In addition, antibody production under restraint stress decreased significantly in aged mice when compared with young mice. No IL-4, IFN-gamma, IL-10 or IL-1 beta were detected in sera from non-stressed or stressed aged mice. Aging exacerbates the immunosuppressive role of acute restraint stress in antigen-specific antibody production in mice.
    Allergology International 02/2009; 58(1):119-24.
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    ABSTRACT: Interactions between eosinophils and monocytes after lipopolysaccharide inhalation are yet to be investigated. The mechanism of eosinophil activation induced by lipopolysaccharide in the presence of monocytes was investigated. Expression of ICAM-1 and Mac-1 on eosinophils was evaluated after lipopolysaccharide stimulation in the presence of monocytes or monocyte culture supernatants. Cytokines in the supernatant of lipopolysaccharide-stimulated monocytes were measured using a cytokine array. Expression of ICAM-1 and Mac-1 on eosinophils was up-regulated after lipopolysaccharide stimulation in the presence of monocytes or monocyte culture supernatant. Lipopolysaccharide induced secretion of ENA-78, GMCSF, GRO, IL-1 beta, IL-6, IL-10, MCP-1, TNF-alpha and MIP-3 alpha from monocytes. The up-regulation of ICAM-1, but not Mac-1, on eosinophils was attenuated by anti-TNF-alpha neutralizing antibody. Monocyte-derived TNF-alpha plays an important role in the up-regulation of ICAM-I on eosinophils induced by lipopolysaccharides.
    Allergology International 02/2009; 58(1):103-10.
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    ABSTRACT: IgA deficiency (IgAD) is the most common immunodeficiency, however the pathogenesis in most cases of IgAD is unknown. There are 2 subclasses of IgA, IgA1 and IgA2, and its heavy chains are encoded by 2 different genes, the alpha1 and alpha2 genes. To investigate the molecular pathogenesis of IgA deficiency, it is important to evaluate each of the expressions of IgA1 and IgA2 separately. In this study, we report on the reverse transcriptase (RT)-PCR method in which alpha1 and alpha2 mRNAs can be separately evaluated. This method is based on electrophoretic separation using the difference of 39 bases between alpha1 and alpha2 mRNAs. Three selective, 5 partial and 2 secondary IgAD patients were examined. In the 3 selective IgAD patients, no alpha1 or alpha2 mRNA expression was detected. In the 5 partial IgAD patients, various alpha1 and alpha2 mRNA expression patterns were found. One of the partial IgAD patients showed only alpha2 gene expression, but not alpha1 gene expression, and was found to show an alpha1 gene deletion together with gamma 2 and epsilon gene deletions. His plasma IgA2 level was within the normal range. Patients with an alpha1 gene deletion can be considered as having partial IgAD. Using this method, we identified the second case of alpha1 gene deletion in Japan, and classified IgAD patients on the basis of alpha1 and alpha2 expression.
    Allergology International 02/2009; 58(1):111-7.
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    ABSTRACT: Basophils comprise the smallest population in human peripheral blood leukocytes. The role of basophils in the pathogenesis of allergic diseases has long been obscure, although their accumulation and activation in tissues have suggested their potential importance. Recent advances in the field of basophil biology have indicated that cytokines and chemokines are the primary regulators of basophil functions. In addition, various functions of these cells seem differently modulated. The evidence strongly supports the notion that basophils exposed to these substances and allergens will behave as unique effector cells that presumably play proinflammatory roles in type I allergic reactions.
    Allergology International 02/2009; 58(1):1-10.
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    ABSTRACT: The addition of leukotriene modifier (LM) may be a useful approach for uncontrollable asthma despite treatment with inhaled corticosteroid (ICS), especially in asthmatics comorbid with allergic rhinitis (AR), although little is known about its molecular mechanism. We evaluated the additive effects of LM with ICS on pulmonary function and airway inflammation in asthmatics with or without AR. Eighteen uncontrolled steroid-treated asthmatics, nine with and nine without AR, were enrolled. Spirometry, peak expiratory flow (PEF) measurements, and exhaled breath condensate sampling were performed before and 8 weeks after LM administration. The lowest PEF over the course of one week, expressed as a percentage of the highest PEF (Min%Max PEF), was used as an index of fluctuation of the airway caliber. Airway cytokine expression was analyzed with a protein array. A significant improvement in forced expiratory volume in one second as a percentage of the predicted value (%FEV(1)) and Min%Max PEF was seen in the subgroup of asthma with AR. Although there was no significant difference in the baseline cytokine values between the groups, the exhaled RANTES level was significantly reduced by LM in the asthma with AR group. The changes in the RANTES level were significantly related to the changes in the %FEV(1) and Min%Max PEF values. LM caused a greater improvement in pulmonary function and airway inflammation in asthmatics with AR. The RANTES-mediated pathway may be involved in the improvement of the airflow limitation and airway lability by LM additive therapy in asthmatics receiving steroid therapy.
    Allergology International 02/2009; 58(1):89-96.
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    ABSTRACT: Histamine is known to have immunoregulatory roles in allergic reactions through histamine receptor 1 (H1R), H2R, H3R and H4R. However, its role in goblet cell hyperplasia in the airways of asthma patients is yet to be clarified. This study was designed to examine the role of histamine in goblet cell hyperplasia using histamine-deficient mice (Hdc-/- mice) with allergic airway inflammation. Wild-type and Hdc-/- C57BL/6 mice were sensitized with ovalbumin (OVA). After a 2-week exposure to OVA, goblet cell hyperplasia was evaluated. Cell differentials and cytokines in BALF were analyzed. The mRNA levels of MUC5AC and Gob-5 gene were determined quantitatively. The number of eosinophils in BALF increased in both the sensitized wild-type mice and Hdc-/- mice with OVA inhalation. In addition, the numbers of alveolar macrophages and lymphocytes in BALF increased significantly in the sensitized Hdc-/- mice with OVA inhalation compared to the wild-type mice under the same conditions. The concentrations of Interleukin-4 (IL-4), IL-5, IL-13, Interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha) and IL-2 in the BALF all increased significantly in both groups compared to those exposed to saline. In particular, the concentration of TNF-alpha in the Hdc-/- mice exposed to OVA was significantly higher than that in the wild-type mice under the same conditions. The mRNA levels of Gob-5 and MUC5AC, and the ratio of the goblet cells in the airway epithelium significantly increased in Hdc-/- mice exposed to OVA compared to wild-type mice. These results suggested that histamine may play a regulatory role in goblet cell hyperplasia in allergic airway inflammation.
    Allergology International 02/2009; 58(1):125-34.
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    ABSTRACT: Basophils and mast cells are major players in the progression of allergic disorders. Although both cell types originate from hematopoietic stem cells, their lineage commitment pathways and mechanisms have been unsolved issues in hematology. Recent advances in the multicolor FACS system enable the prospective isolation of progenitor populations whose readouts are restricted to basophil and/or mast cell lineages. These newly-isolated progenitor subsets are helpful to understand the developmental machinery of basophil and mast cell lineages, leading to the possible exploitation of a novel therapeutic strategy for allergic and autoimmune disorders. In this review, we summarize the recent progress in our understanding of the basophil/mast cell ontogeny on a cellular basis.
    Allergology International 02/2009; 58(1):21-8.
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    ABSTRACT: As patients share in the decision-making process regarding treatments they receive, it is important that they can discriminate between reliable and unreliable sources of information about potential treatments. In this study, health professionals and patients were asked to assess the reliability of information contained in pamphlets on treatments for asthma and atopic dermatitis using a new Japanese translation of an instrument called DISCERN. The scores given by both groups were analyzed to assess inter-rater agreement. The same DISCERN instrument was used by health professionals to evaluate websites on treatments for atopic dermatitis and the degree of inter-rater agreement was assessed again. There was a greater inter-rater agreement between health professionals than between patients. When health professionals used the instrument to evaluate websites, the final rankings given were consistent between different raters, showing good inter-rater agreement. We conclude that DISCERN is useful for evaluating the reliability of medical information both in pamphlets and on the internet, although it is used more effectively by health professionals than by patients. Further studies are needed on the use of DISCERN by patients in evaluating websites containing medical information.
    Allergology International 02/2009; 58(1):141-5.
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    ABSTRACT: The prevalence of patients with chronic rhinosinusitis (CRS) refractory to traditional therapy appears to be on the increase. In these cases, CRS tends to be associated with bronchial asthma (BA), especially, aspirin-intolerant asthma (AIA). On the other hand, arachidonic acid metabolites have been extensively investigated in the pathogenesis of BA. We sought to assess the role of prostaglandin D(2) (PGD(2)) and prostaglandin E(2) (PGE(2)) in the recalcitrant pathophysiology of CRS. Samples were prepared from the nasal polyps and mucosa of 40 patients undergoing endoscopic sinus surgery (ESS) at our hospital. The nasal polyp specimens obtained from the patients with CRS were divided into three groups, as follows: the CRS-AIA group, consisting of specimens obtained from patients with CRS complicated by AIA, the CRS-ATA group, consisting of specimens obtained from patients with CRS associated with aspirin-tolerant asthma (ATA), and the CRS-NA group, consisting of specimens obtained from CRS patients without BA. PGD(2) and PGE(2) were extracted from the specimens and quantified. The concentrations of PGD(2) were significantly higher in the nasal polyps of the CRS-ATA group. The concentrations of PGE(2) were lowest in the nasal polyps of the CRS-AIA group. The PGD(2)/PGE(2) ratio was highest in the CRS-AIA group. It has previously been reported that CRS complicated by AIA is most likely to be characterized by repeated remissions and relapses, and is thus the most intractable. We may therefore say that the PGD(2)/PGE(2) ratio reflects the intractable nature of CRS.
    Allergology International 01/2009; 57(4):429-36.
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    ABSTRACT: A type-IV-allergic reaction to German camomile (Matricaria chamomilla) in a form of allergic contact dermatitis is not unusual. However, only a few cases of anaphylactic reaction to camomile have been described in the literature. We present the case of a 38-year-old Caucasian man who developed an episode of severe anaphylaxis with generalized urticaria, angioedema and severe dyspnoea one hour after consuming camomile tea. Laboratory examination demonstrated a total serum IgE of 123 kU/l with specific IgE against camomile (4.94 kU/l, class 3). Skin prick test and labial provocation test with camomile showed a strong positive reaction. Our case confirms the presence of a type-I allergy to orally ingested camomile and indicates that the incidence and risk may be underestimated. Additional response to mugwort and pollen-derived food allergens should be evaluated in patients sensitised to camomile due to a higher incidence of allergic cross-reactivity.
    Allergology International 01/2009; 58(1):135-6.
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    ABSTRACT: We have previously shown that short-course treatment with Amb a 1-immunostimulatory phosphorothioate oligonucleotide conjugate (AIC) before the ragweed season modifies the response of the nasal mucosa to allergen challenge in ragweed-sensitive patients by increasing Th1 cytokines and decreasing both Th2 cytokines and eosinophilia after the ragweed season. The effect of AIC immunotherapy on CD4+CD25+ T cell expression in the nasal mucosa is unknown. To determine the in vivo effect of short-course AIC immunotherapy on CD4+CD25+ regulatory T cells in the nasal mucosa of ragweed-sensitive subjects. 19 ragweed-sensitive patients with allergic rhinitis were randomly assigned to receive either 6 escalating doses of AIC (0.06-12microg; n = 12) or placebo (n = 7) at weekly intervals immediately before the 2001 ragweed season. Nasal biopsies were taken at baseline prior to immunization and again post immunization 24 hours after ragweed allergen challenge at the start and end of the ragweed season. The expression of T regulatory cells, IL-10 and TGF-beta was assessed at each time point by immunohistochemistry. The numbers of allergen-induced CD4+-, CD4+CD25+-, IL-10- and TGF-beta-positive cells in the nasal mucosa after AIC immunization before the ragweed season did not differ between the two groups. Repeat challenge after the ragweed season led to a significant increase in CD4+CD25+ cells in AIC-compared with placebo-treated subjects. A trend toward an increase in IL-10-positive cells in the AIC-treated group did not reach statistical significance. Short-course AIC immunotherapy increases CD4+CD25+ regulatory T cell infiltration in the nasal mucosa following allergen challenge after seasonal ragweed-pollen exposure.
    Allergology International 01/2009; 57(4):377-81.
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    ABSTRACT: While interleukin-18 (IL-18) plays an important role in the innate and adaptive immune responses, it can also cause severe allergic inflammatory reactions. Thus it is a molecule currently being targeted for therapy. The natural intrinsic inhibitor of IL-18 receptor activation, IL-18 binding protein (IL-18BP), shows a great potential for the treatment of allergy. Expression and purification of recombinant human IL-18BP (rhIL-18BP) were performed using the baculovirus system to develop a therapeutic molecule for the treatment of IL-18-related diseases and to investigate the structural basis of its inhibitory mechanism. Purified rhIL-18BP potently inhibited the production of interferon-gamma by peripheral blood mononuclear cells in the presence of lipopolysaccharide and by human myelomonocytic KG-1 cells in the presence of IL-18 (IC50 = 0.4 nM). Surface plasmon resonance showed a high affinity (Kd = 0.46 nM) for rhIL-18BP in binding hIL-18. Structural analysis indicated that the stoichiometry between IL-18 and IL-18BP is 1 : 1 in solution and the model structure of the complex suggests that the key residues on IL-18 (L5, K53, S55) and the estimated key residues on IL-18BP (F93,Y97, F104) could have interactions. The structural mechanism of IL-18BP inhibition might be a competition for Site 2 on rIL-18 so that IL-18BP can prevent IL-18 receptor alpha from binding to Site 2 and inhibit IL-18 receptor activation. IL-18BP has unique features with respect to its structure, binding mode and inhibitory mechanism. It is a molecule that has a great potential for the therapy of allergy.
    Allergology International 01/2009; 57(4):367-76.
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    ABSTRACT: The therapeutic use of Kampo medicine, Sho-seiryu-to (SST) in allergic disorders is well known. As histamine plays a central role in allergic diseases, it is possible that SST affects the allergy-related histamine signaling. In this study, we investigated the effect of SST on allergy-related histamine signaling in the nasal mucosa of toluene 2, 4-diisocyanate (TDI)-sensitized nasal allergy model rats. Six-week-old male, Brown Norway rats were sensitized for 2 weeks with 10 microl of 10% TDI, and after a 1 week interval, provocation was initiated with the same amount of TDI. SST (0.6g/rat) was given orally 1 hour before TDI treatment began for a period of 3 weeks. Nasal symptoms were scored for 10 minutes immediately after TDI-provocation. The genes expression in nasal mucosa was determined using real-time quantitative RT-PCR. SST significantly suppressed TDI-induced nasal allergy-like symptoms. TDI provocation showed a significant up-regulation of histamine H(1) receptor (H1R) and histidine decarboxylase (HDC) gene expressions. Prolonged pre-treatment of SST significantly suppressed the mRNA levels of H1R and HDC that was up-regulated by TDI. SST also suppressed TDI-induced interleukin (IL)-4 and IL-5 mRNA elevation. However, SST showed no significant effect for TDI-induced mRNA elevation of IL-13. These results demonstrate that SST alleviates nasal symptoms by the inhibition of histamine signaling through suppression of TDI-induced H1R and HDC gene up-regulation. SST also suppresses cytokine signaling through suppression of IL-4 and IL-5 gene expression. Suppression of histamine signaling may be a novel mechanism of SST in preventing allergic diseases.
    Allergology International 01/2009; 58(1):81-8.

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