Allergology International最新文献

Perioperative anaphylaxis (POA) is one of the most critical acute complications in anesthesia practice, characterized by rapid onset, diagnostic complexity, and potentially fatal outcomes. Despite global improvements in anesthesia safety, the unpredictable nature of anaphylaxis continues to challenge clinicians. The Japanese Epidemiologic Study for Perioperative Anaphylaxis (JESPA) established the first nationwide, prospective surveillance system for POA, providing valuable insights into the epidemiology and mechanisms of POA in Japan. Large-scale studies from multiple countries, including the United Kingdom's National Audit Project 6 (NAP6) and France's Groupe d'Étude des Réactions Anaphylactiques Périopératoires (GERAP), have reported similar incidence rates, at approximately 1 in 5000 to 10,000 general anesthesia cases, indicating that POA is a rare but consistently serious global event. In Japan, JESPA confirmed a comparable frequency, identifying neuromuscular blocking agents (NMBAs), antibiotics, and sugammadex as major culprits causing anaphylaxis. Notably, the frequency of sugammadex-induced anaphylaxis is higher in Japan, likely reflecting its extensive clinical use. POA involves both immunologic and non-immunologic pathways, culminating in mast cell activation and mediator release. Its presentation, primarily hypotension and bronchospasm, is often masked under anesthesia, complicating its recognition. Diagnosis requires integrating clinical findings, measuring tryptase using the European Academy of Allergy and Clinical Immunology (EAACI) consensus formula (1.2 × baseline + 2 ng/mL), and identifying causative drugs via skin testing, basophil activation tests (BATs), or drug provocation tests (DPTs). Future priorities include expanding access to tryptase testing, strengthening multidisciplinary collaboration, and promoting anesthesiologist-led allergy investigations to enhance diagnostic precision and patient safety in perioperative care.

Background: Lysophosphatidic acid (LPA) and its receptor LPA1 have been implicated in tissue inflammation and fibrosis; however, their role in mucus overproduction remains unclear. Pulmonary neuroendocrine cells (PNECs), which are rare airway epithelial cells, contribute to mucus overproduction and immune modulation. In this study, we investigated the role of the LPA/LPA1 receptor axis in goblet cell hyperplasia and mucus overproduction, as well as the contribution of PNECs, using a chronic mouse model of bronchial asthma.

Methods: A chronic mouse model of asthma was established by sensitization and challenge with the house dust mite antigen Dermatophagoides pteronyssinus (Dp), with or without treatment using the LPA1 antagonist AM095. Airway hyperresponsiveness, histopathology, mediator concentrations, and molecular expression in lung homogenate supernatants were evaluated. Lysophospholipid levels and low-molecular-weight metabolites were analyzed using liquid chromatography-tandem mass spectrometry (LC-MS/MS).

Results: Lung LPA 22:5 levels were elevated in Dp-challenged mice. LPA1 receptors were co-localized with PNECs in the lung. Treatment with AM095 reduced goblet cell hyperplasia by inhibiting the production of gamma-aminobutyric acid (GABA) and calcitonin gene-related peptide (CGRP) by PNECs. It also suppressed arginase 1 and polyamine production in CGRP-stimulated M2 macrophages. AM095 did not affect eosinophil extracellular trap (EET) formation in bronchoalveolar lavage fluid, which activates PNECs.

Conclusions: The LPA/LPA1 axis promotes goblet cell hyperplasia through PNEC activation and downstream GABA and CGRP signaling in a chronic asthma model. LPA1 antagonism may represent a potential therapeutic strategy for controlling mucus overproduction in asthma.

Background: This large-scale crowdsourced observational study investigated the association between yellow dust, particulate matter 2.5 (PM2.5), and hay fever symptoms using the AllerSearch smartphone application.

Methods: Participants with hay fever were divided into four groups based on combinations of high and low pollen and PM2.5/yellow dust dispersion levels. Nine hay fever symptom scores and quality of life (QoL) scores were compared among the groups. Multivariate analysis evaluated independent associations between pollen and PM2.5/yellow dust dispersion levels and hay fever symptom and QoL scores. Risk factors for individuals experiencing worsening hay fever symptoms during PM2.5/yellow dust dispersion were evaluated using multivariate logistic regression analysis.

Results: This analysis included 6468 participants. All hay fever symptom scores except "ear and/or mouth itching," and all QoL scores were significantly higher in the "low pollen and moderate-to-high PM2.5/yellow dust" group versus the "low pollen and low PM2.5/yellow dust" group. PM2.5/yellow dust levels independently associated with worsening of hay fever symptom and QoL scores, except for "ear and/or mouth itching." Being a woman (P = 0.010), a history of atopic dermatitis (P = 0.013), bronchial asthma (P = 0.046), dry eye disease (P = 0.048), oral medication (P = 0.009) and air purifier use (P = 0.043) were significant risk factors for worsening hay fever symptoms during PM2.5/yellow dust dispersion.

Conclusions: Our findings suggest that PM2.5 and yellow dust exacerbated hay fever symptoms independent of pollen exposure, with distinct symptom profiles.