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Background: Despite the development of biologics for severe asthma, individuals with uncontrolled status persist, posing a significant social problem. This multicenter prospective study aimed to identify factors associated with the uncontrolled status of patients with severe asthma in the biologic era assessed using the Asthma Control Questionnaire (ACQ)., Methods: Subjects with severe asthma diagnosed by respiratory specialists were enrolled from 11 hospitals. Clinical data and questionnaires were collected. We compared controlled (ACQ-5 <1.5) with uncontrolled severe asthma (ACQ-5 ≥1.5) and assessed factors linked to uncontrolled severe asthma using logistic regression analysis., Results: One hundred fifty-four patients were analyzed (median age, 66 years; 62.3 % female; 52.6 % administered biologics). Among them, 56 patients (36.4 %) had uncontrolled severe asthma (ACQ-5 ≥1.5). The uncontrolled group had more frequent exacerbations (≥2 times in the previous year) and elevated blood neutrophil counts compared with the controlled group. Factors associated with uncontrolled status were analyzed in the overall population, with patients stratified into two groups: those receiving biologics and those not receiving biologics. Multivariate analysis revealed that frequent exacerbations and elevated blood neutrophil counts were associated with uncontrolled status in the overall population and in patients without biologics, whereas elevated blood neutrophil counts were significantly associated with uncontrolled status in patients receiving biologics., Conclusion: Elevated blood neutrophil counts and frequent exacerbations were independently associated with uncontrolled severe asthma. Specifically, elevated blood neutrophil counts were a significant factor related to uncontrolled status irrespective of biologics, suggesting their potential utility as a biomarker in the biologic era., Competing Interests: Declaration of competing interest Noriyuki Enomoto has received grants from Boehringer Ingelheim. Toshihiro Shirai received lecture fees from AstraZeneca, Sanofi, Glaxo Smith Kline, Kyorin, Novartis, and Boehringer Ingelheim. These disclosures did not influence the work reported in this paper. The other authors declare no competing interests., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Background: Follicular helper T (Tfh) cells represent a unique subset of helper CD4 + T cells in lymphoid follicles. Recently, Tfh cells were shown to play an important role in asthma through B cell differentiation. Conventional lung DCs are classified into two major subsets: conventional type 1 (cDC1) and type 2 (cDC2). Although the two subsets are different in driving particular T cell responses, the subset that induces Tfh cells in the asthmatic lung primarily has yet to be fully elucidated., Methods: We evaluated Tfh cells, defined by the expression of CD4 and CXCR5, in HDM-challenged mice. Next, we characterized cDC1 and cDC2 purified from antigen-primed lung and examined their Tfh cell-inducing capacity. Additionally, the ability of lung DC-induced Tfh cells to cause germinal center B (GCB) cells to produce antigen-specific IgE was assessed., Results: In HDM-challenged mice, Bcl-6-expressing Tfh cells were significantly increased in the mediastinal lymph nodes. Lung cDC2, but not lung cDC1, increased after HDM priming, and cDC2 secreted larger amounts of IL-6 with higher ICOS-L expression than cDC1. In the co-cultures with OVA-specific naïve CD4 + T cells, cDC2 from OVA-primed lung induced Bcl-6-expressing Tfh cells more efficiently, together with larger amounts of IL-6 and IL-21, than cDC1. Blockage of IL-6 or ICOS-L significantly reduced Tfh cell induction. Finally, cDC2-induced Tfh cells enabled GCB cells to produce OVA-specific IgE., Conclusions: In asthmatic lung, cDC2 is the primary DC subset responsible for Tfh cell differentiation and plays an important role in humoral immunity in asthma by inducing Tfh cells., (Copyright © 2021 Japanese Society of Allergology. Production and hosting by Elsevier B.V. All rights reserved.)

We herein report a 38-year-old woman with breast cancer who developed Pneumocystis jirovecii pneumonia (PCP) during neoadjuvant dose-dense chemotherapy combined with dexamethasone as antiemetic therapy. Chest computed tomography showed bilateral ground-glass opacities and consolidation. The serum β-D-glucan levels were elevated, and P. jirovecii DNA was detected from the bronchoalveolar lavage fluid by polymerase chain reaction. Her clinical findings improved with trimethoprim/sulfamethoxazole and adjunctive steroid therapy. Clinicians must be mindful of the manifestations of PCP in non-human immunodeficiency virus (HIV)-infected immunocompromised patients and include the possibility of PCP in the differential diagnosis when confronted with breast cancer on dose-dense chemotherapy showing diffuse lung disease.

Invasion of the endobronchial mucosa by cancer cells is frequently seen in small cell lung cancer (SCLC), but an intraluminal polypoid growth pattern is extremely rare. We herein describe the case of a 69-year-old woman with limited-stage SCLC who had a pedunculated mass in the orifice of the right upper bronchus. Thin-section CT of the lung showed an endobronchial protruding mass accompanied by tubular and branching opacities (the so-called finger-in-glove sign) in the right upper lobe bronchus, which were enhanced by contrast media. She responded well to chemotherapy with concurrent radiation therapy. Although very rare, SCLC patients can have intraluminal polypoid growth, as was observed in this case.

Bronchoscopic findings often show mucoid impaction in patients with allergic bronchopulmonary aspergillosis (ABPA); however, endobronchial mucosal nodular lesions have not been reported. We herein present the first such case of a 52-year-old woman with ABPA with endobronchial mucosal nodular lesions. The endobronchial lesions were located in the orifice of the mucoid impaction, and disappeared after 4 weeks of treatment with prednisolone and itraconazole. Aspergillus fumigatus was cultured from bronchial lavage fluid collected from the site of mucoid impaction. Based on these clinical findings, we speculate that the bronchial lesions were caused by an inflammatory and allergic reaction to Aspergillus antigens., Competing Interests: I declare on behalf of my co-authors and myself that we do not have any conflict of interest to declare., (© 2019 The Authors.)

An 84-year-old man visited our hospital with a prolonged productive cough. Chest computed tomography showed a thick wall cavity and bilateral consolidations. Laboratory findings revealed peripheral blood eosinophilia, increased total IgE and elevated myeloperoxidase anti-neutrophil cytoplasmic antibody. Specific IgE and IgG antibodies and an immediate skin reaction against Aspergillus showed positive results. The histological findings of the lung parenchyma were compatible with eosinophilic pneumonia and bronchial biopsy showed eosinophilic vasculitis. Bronchoalveolar lavage fluid culture yielded Aspergillus fumigatus . These results met the diagnosis criteria for both allergic bronchopulmonary aspergillosis (ABPA) and eosinophilic granulomatosis with polyangiitis (EGPA). This case thus suggests that A. fumigatus might be a pathogen common to both diseases, and prolonged exposure to A. fumigatus in some patients with ABPA may promote progression to EGPA.

Severe community-acquired pneumonia (CAP) caused by methicillin-resistant Staphylococcus aureus (MRSA) is relatively rare and is usually associated with rapid progression to death. Here, we report the complete genome sequence of the MRSA strain JMUB3031, which was isolated from a patient with fatal CAP.

Diffuse alveolar hemorrhage, a life-threatening disease, can complicate various conditions. We herein describe, for the first time, a patient with diffuse alveolar hemorrhage caused by exposure to organic dust. A 49-year-old woman who worked as a cantaloupe farmer in a greenhouse was referred to our hospital for sudden onset of dyspnea 3 h after exposure to organic dust. A chest X-ray and computed tomography scan performed on admission showed diffuse ground-glass opacities in both lung fields. Suspecting hypersensitivity pneumonitis, fiberoptic bronchoscopy was performed. Mucopurulent sputum was present in the trachea and both bronchi, and bronchoalveolar lavage revealed a progressively bloody return, typical of diffuse alveolar hemorrhage. Based on the history and bronchoscopy findings, she was diagnosed with diffuse alveolar hemorrhage following exposure to organic dust and was treated with antibiotics and corticosteroids. Diffuse alveolar hemorrhage should be considered in the differential diagnosis of diffuse ground-glass opacities observed on radiographs in farmers following exposure to organic dust.

A 64-year-old man who had been exposed to asbestos was referred to our hospital for a detailed examination of left pleural effusion. A laboratory examination of the urine and blood revealed nephrotic syndrome. A thoracoscopic examination did not yield a definitive diagnosis. Twenty months later, a left pleural tumor became apparent, and the patient died of respiratory failure and cachexia. An autopsy revealed epithelioid malignant pleural mesothelioma. The glomeruli appeared normal under light microscopy. A review of the English literature revealed only three reports of malignant mesothelioma associated with minimal-change nephrotic syndrome. The natural course of malignant mesothelioma with nephrotic syndrome has not been previously reported.