Thymic stromal lymphopoietin (TSLP) is an IL-7-like cytokine initially identified in the culture supernatant of a thymic stromal cell line. Highly expressed in the epidermis in skin lesions of atopic dermatitis patients, TSLP was subsequently found to be a critical factor linking responses at interfaces between the body and environment (skin, airway, gut, ocular tissues, and so on) to Th2 responses. Recent studies have revealed that various cell types other than epithelial cells and epidermal keratinocytes (such as mast cells, airway smooth muscle cells, fibroblasts, dendritic cells, trophoblasts, and cancer or cancer-associated cells) also express TSLP. Environmental factors such as Toll-like receptor ligands, a Nod2 ligand, viruses, microbes, allergen sources, helminths, diesel exhaust, cigarette smoke, and chemicals trigger TSLP production. Proinflammatory cytokines, Th2-related cytokines, and IgE also induce or enhance TSLP production, indicating cycles of amplification. Skin barrier injury, increased epidermal endogenous protease activity, and less epidermal Notch signaling, all of which have been reported in atopic dermatitis, and keratinocyte-specific loss of retinoid X receptors and treatment of skin with agonists for vitamin D receptor in mice induce TSLP production, Th2 response, or atopic dermatitis-like inflammation. The transcription factors NF-κB and AP-1, nuclear receptors, single nucleotide polymorphisms, microRNAs, and the peptidyl-proryl isomerase Pin1 regulate TSLP mRNA expression transcriptionally or posttranscriptionally. This review focuses on events upstream of TSLP production, which is critical in allergic diseases and important in other TSLP-related disorders i.e. production sites, cellular sources, environmental and endogenous triggers and regulatory factors, and regulatory mechanisms of gene expression.

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In an immune system, dendritic cells (DCs) are professional antigen-presenting cells (APCs) as well as powerful sensors of danger signals. When DCs receive signals from infection and tissue stress, they immediately activate and instruct the initiation of appropriate immune responses to T cells. However, it has remained unclear how the tissue microenvironment in a steady state shapes the function of DCs. Recent many works on thymic stromal lymphopoietin (TSLP), an epithelial cell-derived cytokine that has the strong ability to activate DCs, provide evidence that TSLP mediates crosstalk between epithelial cells and DCs, involving in DC-mediated immune homeostasis. Here, we review recent progress made on how TSLP expressed within the thymus and peripheral lymphoid and non-lymphoid tissues regulates DC-mediated T-cell development in the thymus and T-cell homeostasis in the periphery.

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The cytokine TSLP was originally identified in a murine thymic stromal cell line as a lymphoid growth factor. After the discovery of TSLP, extensive molecular genetic analyses and gene targeting experiments have demonstrated that TSLP plays an essential role in allergic diseases. In this review, we discuss the current status of TSLP and its functional role in allergic diseases particularly by focusing on effects of TSLP on haematopoietic cells in mouse models. It is our conclusion that a number of research areas, i.e., a new source of TSLP, effects of TSLP on non-haematopoietic and haematopoietic cells, synergistic interactions of cytokines including IL-25 and IL-33 and a regulation of TSLP expression and its function, are critically needed to understand the whole picture of TSLP involvement in allergic diseases. The mouse models will thus contribute further to our understanding of TSLP involvement in allergic diseases and development of therapeutic measures for human allergic diseases.

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Thymic stromal lymphopoietin (TSLP) has been recently implicated as a key molecule for initiating allergic inflammation at the epithelial cell-dendritic cell (DC) interface. In humans, aberrant TSLP expression is observed in allergic tissues, such as lesional skins of atopic dermatitis, lungs of asthmatics, nasal mucosa of atopic rhinitis and nasal polyps, and ocular surface of allergic keratoconjunctivitis. TSLP is produced predominantly by damaged epithelial cells and stimulates myeloid DCs (mDCs). TSLP-activated mDCs can promote the differentiation of naïve CD4⁺ T cells into a Th2 phenotype and the expansion of CD4⁺ Th2 memory cells in a unique manner dependent on OX40L, one of the tumor necrosis factor superfamily members with Th2-promoting function, and lack of production of IL-12. From a genetic point of view, multiple genome-wide association studies have repeatedly identified the TSLP gene as one of the loci associated with susceptibility to allergic diseases. Thus, TSLP is a rational therapeutic target for the treatment of allergic disorders. Elucidating the mechanisms that regulate TSLP expression and the effects of TSLP on orchestrating the immune response toward a Th2 phenotype is essential for developing anti-TSLP therapy.

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Allergic contact dermatitis caused by contact with lacquer sap and lacquerware affects the welfare of lacquer workers and the lacquerware industry. Many studies of the mechanism of urushiol allergy, including animal models, have been carried out and have established several hypotheses. In order to provide a comprehensive understanding of lacquer allergy, we review recent advances in the research on lacquer allergy including the chemical properties of lacquer lipid components, allergic mechanism analyses, immunological explanations, allergy medications, and the prevention combined with the research results from our laboratory.

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Background: Reducing risk factors, such as exposure to allergens, and stepwise pharmacotherapy to achieve and maintain control of asthma are the mainstay of asthma care. The purpose of this study was to clarify the effect of exposure and sensitization to indoor allergens, including house dust mites, cats, and dogs, on the asthma control level.
Methods: Dust samples were collected from the mattresses of 101 adult asthma patient homes and the Dermatophagoides mite group 1 (Der 1), Fel d 1, and Can f 1 concentrations were measured using ELISA. Sensitization was determined by positive specific IgE antibodies. The Asthma Control Test (ACT), lowest peak expiratory flow (PEF) during 1 week expressed as a percentage of the highest PEF (Min%Max PEF), and spirometry were measured for the assessment of asthma control. Univariate and multivariate regression analyses were used to assess the relationships.
Results: Sixty-nine patients were exposed to high levels (>10 μg/g dust for Der 1 and Can f 1 and >8 μg/g dust for Fel d 1) of 1 or more allergens and 39 patients were sensitized to at least one allergen. Multivariate logistic regression analyses revealed that the FEV₁ (% of predicted value) was associated with low ACT scores (≤19) and that the number of highly exposed allergens and inhaled corticosteroid dose were associated with a low level of Min%Max PEF (<80%).
Conclusions: The level of exposure to multiple indoor allergens, but not sensitization, is associated with the asthma control level determined by PEF variation.

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Background: Atopic dermatitis (AD) and Japanese cedar pollinosis (JCP) are common chronically allergic diseases associated with the activation of T-helper 2 cells. Recent studies have shown that polymorphisms in the genes for IL-4 receptor α chain (IL4RA) may contribute to susceptibility of AD and JCP, although the differences in the involvements of loci of IL4RA gene between AD and JCP are unclear. In this study, we investigated the role of polymorphisms in IL-4RA gene in conferring susceptibility to the development of AD and/or JCP using a family analysis and an association analysis in a Japanese population.
Methods: Five polymorphisms in the IL-4RA gene, C-3223T, T-1914C, T-890C, Ile50Val and Glu375Ala, have been genotyped using PCR-based methods in 75 trios families, including 15 AD families, 30 JCP families, and 30 families with combination of AD and JCP in the family analysis. Forty-five AD, 60 JCP and 125 control children constituted the association study.
Results: The transmission disequilibrium test showed that the allele of Ile50 was significantly transmitted to children with JCP alone (p < 0.05). Haplotype analysis showed that the -3223T/Ile50 haplotype was preferentially transmitted to both AD (p < 0.01) and JCP children (p < 0.01), while that the C-3223/Ile50 haplotype was preferentially transmitted to only JCP children (p < 0.01). The association study showed that -3223T and haplotype of -3223T/Ile50 were associated with AD children, but not with JCP. Ile50 was associated with both AD and JCP.
Conclusions: Our data suggest that -3223T and the -3223T/Ile50 haplotype were risk factors for AD. Ile50 allele seems to be involved in both JCP and AD. Interactions of the IL-4RA loci may play a role both conferring susceptibility and modulating severity of AD.

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Background: The present study aimed to illustrate clinical characteristics of spirometric measures and allergy sensitisation among young atopic adults who reported wheezing episodes before adulthood but were not diagnosed with asthma by physicians and have no current wheeze symptoms (self-reported past-wheezers), especially those who exhibited airway hyperresponsiveness (AHR).
Methods: Fifty self-reported past-wheezers were divided into two groups according to AHR to methacholine. Spirometric functions and blood atopic parameters were compared in these groups with those in 25 age-matched atopic adults with a history of childhood asthma diagnosed by specialists but have no current wheeze symptoms (past-asthmatics) and in 60 counterparts without a previous and current wheezing episode (never-wheezers).
Results: Twenty-one of the 50 past-wheezers exhibited AHR (PC₂₀ <8 mg/ml). Levels of spirometric function and allergic sensitization in both past-wheezer groups were intermediate between those in never-wheezers and past-asthmatics. Lower FEV₁ and FEF_25-75 values (% predicted) were observed in self-reported past-wheezers with AHR relative to those without AHR. More blood eosinophils and higher serum levels of total IgE and IgE specific to house dust mites were observed in self-reported past-wheezers with AHR relative to those without AHR.
Conclusions: Our findings raise the possibility that self-reported past-wheezers with AHR might form a distinct subgroup with features similar to past-asthmatics, which is one of the risk groups for adult asthma.

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Background: The pandemic influenza A (H1N1) 2009 [pdm (H1N1) 2009] spread through the world in 2009, producing a serious epidemic in Japan. Since it was suggested early that asthma is a risk factor for an increased severity of the infection, the Japanese Society of Pediatric Allergy and Clinical Immunology (JSPACI) organized a working group for countermeasures, and investigated asthmatic children admitted to the hospitals for pdm (H1N1) 2009 infection.
Methods: An appeal was made on the home page of the JSPACI to medical practitioners to input clinical information about asthmatic and non-asthmatic children (0-19 years) admitted to the hospital with pdm (H1N1) 2009 infection.
Results: A total of 862 children (390 with asthma, and 472 without asthma) from 61 medical centers were registered, and the data of 333 asthmatic children and 388 non-asthmatic children in all were entered in the analyses. The mean age was 7.4 ± 2.9 years in the asthma group and 6.9 ± 3.8 years in the non-asthma group. The percentage of children admitted for respiratory symptoms was significantly higher in the asthma group than in the non-asthma group (p < 0.001). There was no significant difference in the frequency of admission to the ICU or need for mechanical ventilation support between the two groups. No definite trend was detected in the relationship between the severity of asthma and the intensity of asthma attack. Antiviral drugs were administered within 24 hours in about 85% of the patients in both groups.
Conclusions: Asthma may not be a risk factor for severe pdm (H1N1) 2009 infection in children.

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Background: Hypersensitivity pneumonitis (HP) is an immune-mediated lung disease induced by inhalation of numerous antigens. Pathologically, chronic HP tends to show usual interstitial pneumonia (UIP) and fibrotic nonspecific interstitial pneumonia (fNSIP) patterns. Patients with UIP pattern present insidious onset and a risk for acute exacerbations.
Methods: To evaluate the proteomic differences of bronchoalveolar lavage fluid (BALF) between UIP and fNSIP patterns, BALF from seven patients with UIP pattern and four patients with fNSIP pattern was examined using two-dimensional gel electrophoresis and mass spectrometry.
Results: By individually comparing each BALF sample, we found that the protein levels of surfactant protein A (SP-A), immunoglobulin heavy chain α, α-2 heat shock glycoprotein, haptoglobin β, and immunoglobulin J chain were significantly higher in the patients with UIP pattern than those in the patients with fNSIP pattern. In contrast, the protein levels of glutathione s-transferase, vitamin D-binding protein, and β-actin were significantly higher in the patients with fNSIP pattern than those in the patients with UIP pattern. To confirm the results of SP-A in the BALF proteome, we performed enzyme-linked immunosorbent assay in a larger group. The concentrations of SP-A in BALF from the patients with UIP pattern were significantly higher than those from the patients with fNSIP pattern (2.331 ± 1.656 μg/ml vs. 1.319 ± 1.916 μg/ml, p = 0.034).
Conclusions: We identified several proteins that may play roles in the development of pathological differences between UIP and fNSIP patterns of chronic HP.

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Background: There has been an increasing interest in monitoring the fractional concentrations of exhaled NO (FeNO) levels in allergic rhinitis (AR) patients. In the present study, we examined whether the nasal FeNO measurement might reflect the degree of local allergic inflammation as well as subjective symptoms.
Methods: The FeNO measurement was performed using a handheld electrochemical analyzer (NObreath^®) with a nose adaptor. In the cross-sectional study, 56 patients with perennial AR patients, 18 AR patients with bronchial asthma (BA), 12 patients with vasomotor rhinitis, and 30 normal subjects were enrolled. For the follow-up study, 12 seasonal allergic rhinitis (SAR) patients against Japanese cedar and 10 perennial AR patients who underwent laser surgery were examined.
Results: The AR patients and vasomotor rhinitis patients showed significantly higher oral FeNO levels as compared with the normal subjects. The nasal FeNO levels were significantly higher in the perennial AR patients with or without BA than in the normal subjects and vasomotor rhinitis patients. There were positive correlations between the nasal symptom scores and FeNO levels. The SAR patients showed a significant decrease in the nasal FeNO level after the pollen dispersion season. In addition, the therapeutic effects of laser surgery in the AR patients accompanied a significant reduction in the nasal FeNO levels one month after treatment.
Conclusions: The nasal FeNO measurement by NObreath^® is easy to perform and suitable for monitoring AR patients in various treatment modalities. Furthermore, it may have potential usefulness as a tool to improve daily clinical care.

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Background: Wheat is one of the most common causes of food allergies. The exact prevalence of wheat allergy has not been well delineated in Japanese adults.
Methods: We enrolled 935 adults in a cohort study established by Shimane University in order to examine the determinants of lifestyle-related diseases. A screening was conducted by a questionnaire-based examination and a detection of serum omega-5 gliadin-specific IgE. Subjects who tested positive in the questionnaire-based examination and/or the serum omega-5 gliadin-specific IgE test were further examined by detailed interviews and skin prick tests.
Results: A total of 22 subjects were picked up by the screening process, and 17 of these were further examined by secondary testing. Only two subjects were conclusively identified as having wheat allergy.
Conclusions: The prevalence of wheat allergy in Japanese adults was found to be 0.21% by using a combination of questionnaire-based examination, skin prick test and serum omega-5 gliadin-specific IgE test.

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Background: To examine occurrence of cow's milk protein intolerance (CMPI) in newborns that underwent small intestine surgery and the clinical profiles of those newborns with postoperative CMPI, and to evaluate the preventive effects of probiotics on CMPI.
Methods: We retrospectively reviewed from 2000 to 2009, a total of 30 newborns required surgery on their small intestines. All of these patients had received antibiotics to prevent postoperative infection. Since 2005 we adopted a protocol of targeted probiotic therapy prophylaxis.
Results: Eighteen patients received probiotic therapy, while twelve did not. One infant among those eighteen patients and eight patients among those twelve developed CMPI, a significantly lower rate for the group with probiotic therapy than that without it (p < 0.001). Patients with positive cultures for gram positive and gram negative organisms increased in number before and after surgery but then decreased after probiotics treatment. Poor weight gain, gastrointestinal symptoms, and rise in C reactive protein (CRP) levels were observed in all of those nine CMPI patients. Specific IgE antibodies were elevated in four of the nine subjects, and total IgE levels were elevated in seven of them. All CMPI patients had increased level of CRP without proven infections.
Conclusions: CMPI was induced in newborns after surgery on their small intestines and antibiotics treatment with presentation of symptoms that mimic postoperative infection. Development of CMPI in this population possibly involves disruption of intestinal flora. Administration of probiotics can reduce the incidence of CMPI after small intestine surgery. The elevated CRP level may be useful in the diagnosis of CMPI.

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Background: Chronic rhinosinusitis (CRS) is classified in CRS without nasal polyp (CRSsNP) and CRS with nasal polyp (CRSwNP) in western countries, whereas this classification was not common so far in Japan. Studying inflammatory mediators in clearly defined disease subgroups may lead to a better differentiation of chronic sinus diseases.
Methods: Homogenates of sinonasal mucosal tissue from 14 controls, 9 CRSsNP patients, and 19 CRSwNP patients were assayed for transforming growth factor (TGF)-β, interleukin (IL)-5, immunoglobulin E (IgE), Staphylococcus enterotoxin (SAE)-IgE, eosinophil-catioic protein (ECP), myeloperoxidase (MPO), IL-1β, IL-6, and IL-8 by enzyme-linked immunosorbent assay or UNICAP system.
Results: CRSwNP had significantly higher levels of IL-5, IgE, SAE-IgE, and ECP compared with CRSsNP and controls. CRSsNP was characterized by high levels of TGF-β, while CRSwNP showed a Th2 polarization and lower levels of TGF-β. Especially, in CRSwNP samples, 68.4% were eosinophilic (ECP/MPO ratio >1), and 52.6% were SAE-IgE positive. On the other hand, in 9 CRSsNP patients, eosinophilic or SAE-IgE positive sample was only one sample respectively. Additionally, 31.6% of CRSwNP were asthmatic patients, while none of CRSsNP patient was suffering from bronchial asthma.
Conclusions: This study is thought to be the first one that showed the cytokine profiles in Japanese CRSs/wNP similar to those of European CRS. Based on mediator profiles, we suggest that CRSsNP and CRSwNP are distinct disease entities within the group of chronic sinus diseases.

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Background: The character or timing of chronic cough is considered to be unpredictable for diagnosing its cause. However, the associations of cough triggers with cough pathophysiology remains unknown.
Methods: We developed a closed questionnaire listing 18 triggers that were reported by ≥1% of 213 patients in a retrospective survey. Using this questionnaire, patients with cough-predominant or cough-variant asthma (n = 140) and those with non-asthmatic cough (54) were asked whether their cough was induced by the listed triggers. Associations of triggers with causes of cough, airway sensitivity to inhaled methacholine, exhaled nitric oxide (NO) levels, number of sensitizing allergens, and scores from gastroesophageal reflux (GER) questionnaires were examined. Factor analysis was used to categorize variables, including the 12 most common cough triggers, diagnosis of asthmatic cough, airway sensitivity, and exhaled NO levels.
Results: "Cold air" and "fatigue/stress" induced cough more often in asthmatic coughers than in non-asthmatic coughers. "Spices" and "meals" induced cough more frequently in GER-coughers (n = 19). Patients who marked "cold air" as the trigger were more sensitive to inhaled methacholine and showed higher exhaled NO levels than those who did not mark this trigger. The "post-nasal drip" trigger was associated with elevated exhaled NO levels, and this association was mainly exhibited by patients with cough-predominant asthma. The triggers "pollen" and "mold smell" were associated with a number of sensitizing allergens. The number of triggers was weakly associated with GER scores. By factor analysis, "cold air," "fatigue/stress," asthmatic cough, airway hypersensitivity, and elevated NO levels were categorized into the same factor.
Conclusions: Several cough triggers may reflect the pathophysiology of prolonged or chronic cough.

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Background: Human Ca²⁺-activated Cl ion channel 1 (hCLCA1) is expressed in goblet cell hyperplasia in the airway of asthmatics, and murine CLCA3 is associated with antigen-sensitized and IL-13-induced goblet cell metaplasia in mice. However, the role of CLCA in goblet cell degranulation is not fully investigated. Niflumic acid (NFA), a relatively specific CLCA inhibitor, inhibits goblet cell metaplasia, but the effect of NFA on goblet cell degranulation has not been determined in an asthma model.
Methods: Guinea pigs were sensitized with ovalbumin (OA) twice and then challenged with saline, OA, histamine, and one of the Ca²⁺-dependent secretagogues, UTP. The PAS/AB-stained mucus area in the tracheal epithelium was measured with a computer image analysis system, and the morphology of mucus granules was examined by transmission electron microscopy. In the in vitro experiment, goblet cells cultured with IL-13 at the air-liquid interface were stimulated with UTP in the presence or absence of NFA, and the MUC5AC level in cell lysates was measured by ELISA.
Results: The mucus areas were smaller in the OA-, histamine-, and UTP-challenged animals than in the saline-challenged animals. NFA inhibited the decrease in mucus area and morphological changes in mucus granules. UTP caused swelling and exocytosis of mucus granules and MUC5AC secretion by cultured goblet cells, and NFA inhibited these changes.
Conclusions: NFA inhibited the secretory response of mucus granules in an asthma model, suggesting that CLCA may be associated with goblet cell degranulation and that CLCA inhibitors may be useful for the treatment of hypersecretion in asthma.

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Background: Lung function determined by spirometry and the severity of dyspnea correlate weakly in asthma patients. We attempted to determine the risk factors in asthma patients having persistent airway obstruction despite of having only mild subjective symptoms, and to examine the possibility of improving FEV1 by treating asthma on the basis of the bronchodilator change in FEV1.
Methods: We examined asthma patients in their 20s and who visited Sagamihara National Hospital for the first time over a period of four years, by reviewing their clinical records. They underwent tests on the bronchodilator change in FEV1 and a test of airway hyperresponsiveness to histamine dihydrochloride.
Results: One hundred thirty-eight subjects (mean age, 25.6 years; 51 males, 87 females; current smoking, 30.4%; history of childhood asthma, 48.6%) were enrolled. Among them, 18.8% (26/138) showed persistent airway obstruction (postbronchodilator FEV1/FVC (%) <80%). Using the multiple logistic regression model, we found that history of childhood asthma and smoking history were the significant isolated risk factors for persistent airway obstruction. Moreover, we determined that the factors associated with the reversibility of airway obstruction in asthma patients without subjective symptoms were history of childhood asthma.
Conclusions: In this study, patients not undergoing treatment for asthma were examined. History of childhood asthma and smoking history may be the risk factors for persistent airway obstruction in the asthma patients with mild subjective symptoms. Tests on the bronchodilator change in FEV1 should be performed in patients with history of childhood asthma and smoking history, even if they have only mild subjective symptoms.

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Background: Although investigations of the drug aerosols generated from inhaled corticosteroid (ICS) preparations and combined drug preparations provide basic information about inhalation therapy, many clinicians have one-sided data about the precision of drug aerosols from the manufacturer. The present study was conducted to analyze and compare the performances of dry powder inhaler (DPI) devices of ICS and combined drug preparations.
Methods: The particle size of individual aerosols was measured according to the time-of-flight principle in terms of their aerodynamic diameter by using the aerodynamic particle sizer spectrometer Model 3321. Percent aerosolization was measured using only stage #0 and backup filters of the Andersen non-viable sampler model AN-200.
Results: The particle size distribution of aerosols generated from a Turbuhaler^TM and Twisthaler^TM showed a mono-modal distribution of less than 5μm. In contrast, Diskus^TM showed a polydisperse distribution, ranging from 0.5 to 20μm. The percentages of DPI preparations converted into aerosols with a particle size less than 11μm at a suction flow rate of 28.3L/min were 5.7-6.2% for Diskus, 37.5-47.0% for Turbuhaler, and 19.8% for Twisthaler. At a suction flow rate of 60L/min, the conversion percentages for DPI preparations into aerosols with a particle size less than 7.6μm were 5.9-7.5%, 78.2-86.7%, and 43.5%, respectively.
Conclusions: Because in vitro differences in the aerosolization among different DPI devices containing ICS and combined drug preparations were observed, prescribers of these preparations should consider whether the patients will benefit more from the treatment of the central airways versus the peripheral airways.

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Background: In Japan, oral antihistamines are frequently used as the initial treatment for seasonal allergic rhinitis (SAR), and intranasal steroids are added when nasal symptoms worsen. This study aimed to evaluate whether starting treatment with fluticasone propionate nasal spray (FP) from the beginning of pollinosis symptoms and adding fexofenadine hydrochloride tablet (FEX) when SAR is aggravated could achieve improved amelioration of nasal symptoms throughout the pollen season in comparison with a treatment that involves starting with FEX and later adding FP.
Methods: In this pragmatic, randomized, open-label, parallel-group trial, 51 Japanese cedar pollinosis patients (age, 16-85 years) were randomly divided and administered FP 100 mcg twice daily as an initial drug with FEX 60mg twice daily as an additional drug and the same treatment in the reverse order. Nasal symptoms were evaluated in a daily dairy using a 4-point scale. The primary outcome was area under curve of the line representing the daily total nasal symptom score in the pollen season on a graph.
Results: Initial treatment with FP was significantly (P = 0.0015) more effective than initial treatment with FEX in improving the primary outcome. The average daily total nasal symptom score in the initial treatment with FP group was better than that in the initial treatment with FEX group throughout the pollen season.
Conclusions: Initiating treatment with FP and adding FEX might lead to improved outcomes for nasal symptoms in comparison with the same drugs administered in the reverse order.

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Background: Although mucoid impaction of the bronchi (MIB) is a well-known manifestation in allergic bronchopulmonary mycosis (ABPM), when unknown samples or plural eumycetes are cultured from bronchial materials, several problems are encountered which can affect the definitive diagnostic process or successful treatment.
Case Summary: The definitive diagnostic process of two patients [a 58-(Case 1) and a 70-(Case 2) year-old female] with MIB was: 1) to identify the existence of any allergic respiratory disorder, 2) to detect the fungi obtained from bronchial materials, with use of the 28S rDNA sequencing and analysis, 3) to investigate whether the detected fungus was a probable etiologic antigen, and 4) to make the final diagnosis based on the results of the inhalation examinations using the antigenic solution of the fungi. As a treatment strategy, bronchial toilet and low dose itraconazole therapy were planned according to the clinical manifestations of each patient.
Discussion: The two patients with MIB were successfully diagnosed as ABPM caused by Schizophyllum commune (Sc-ABPM) accompanied with hyperattenuating mucoid impaction. The reliability of some allergological makers as a substitution for the bronchoprovocation test should be clarified in near future. Clinical manifestations demonstrated in our cases suggested that the allergic reaction such as eosinophilic bronchoalveolitis spreading around the mucus plug was a primary lesion underlying the Sc-ABPM. The success of the treatment for Sc-ABPM will be achieved by the strategy targeting to fundamental condition and by the control of the disease recurrence by means of effective environmental management.

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Background: Autoimmune pancreatitis is characterized by diffuse swelling of the pancreas and a high serum immunoglobulin (Ig) G4 concentration. Histopathologically, dense infiltration of lymphocytes and IgG4-positive plasma cells with fibrosis are seen in the pancreas. Although allergic diseases complicating autoimmune pancreatitis have been reported, the clinical features of bronchial asthma complicated by autoimmune pancreatitis remain unclear.
Case Summary: We report three cases of bronchial asthma preceding the onset of type 1 autoimmune pancreatitis by 3 months to 30 years. All three cases were males with high serum IgG, IgG4, and IgE concentrations. The radioallergosorbent tests were positive for common allergens such as mites and house dust. One case had a pulmonary manifestation that proved to be an inflammatory pseudotumor of the lung with an accumulation of IgG4-positive plasma cells. The asthma symptom was ameliorated by oral prednisolone therapy for autoimmune pancreatitis, and when the corticosteroid doses were reduced, asthma became worse in all three cases.
Discussion: It is possible that atopy and increased Th2 cell activity are related to a higher coincidence of IgG4-related diseases such as type 1 autoimmune pancreatitis. Because the present cases are few in number, further studies are necessary.

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