The common causes of epistaxis in children are mostly local mucosal dryness, trauma, or inflammation, while epistaxis caused by leech infestation is clinically rare and easily overlooked. This article reports a case of epistaxis in a child due to leeches and, combined with a literature review, analyzes its clinical characteristics and key points of diagnosis and treatment. Children often present with recurrent unilateral epistaxis, nasal obstruction, and a feeling of insect crawling, and most have a history of exposure to natural water. The diagnosis of epistaxis due to nasal hirudiniasis mainly relies on the detection of leeches through anterior rhinoscopy or endoscopic examination, and it is necessary to differentiate it from the common causes of epistaxis. The primary treatment is the thorough removal of leeches, supplemented by nasal irrigation or anti-infective measures. This study emphasizes that in endemic areas or in the context of relevant exposure history, leech infestation should be included in the differential diagnosis of intractable epistaxis in children to improve clinical vigilance and avoid misdiagnosis or missed diagnosis.

BACKGROUND:Nasal polyps (NP) are common upper respiratory conditions with diverse inflammatory subtypes influencing clinical features and prognosis. Manual counting of inflammatory cells in microscopic images (MI) is laborious and subjective, limiting diagnostic precision and treatment decisions. METHODS:A total of 2457 slides from 20 hospitals were used to develop an AI-based NP subtype diagnosis system (NPSS). NPSS-MI was built using 1047 slides (15,705 MIs) annotated by pathologists. NPSS-WSI was trained on 1410 slides (21,150 images) combining PA-P2PNet for cell detection and U-KAN for region segmentation. Three-dimensional reconstruction (3DNP) using registration and point cloud analysis enabled spatial quantification of inflammatory cells. Twelve pathologists evaluated NPSS accuracy and efficiency on 200 slides, and recurrence prediction models were developed using logistic regression in a 131-patient cohort. RESULTS:NPSS achieved performance with a weighted average F1-score of 0.809 for cell detection and an intersection over union (IoU) of 0.827 for region segmentation with an internal dataset. External dataset performance showed an F1-score of 0.792 and an IoU of 0.815. Forty randomly accumulated MIs were approximated WSI results. NPSS-MI and NPSS-WSI reached accuracies of 90% and 91%, reducing diagnostic time from 193 to 8 s and from 10,450 to 250 s, respectively. Junior pathologists using NPSS improved accuracy from 50% to 89%. Inflammatory cells showed distinct spatial patterns in 3DNP. NPSS-WSI prognostic model outperformed the MI-based model (AUC 86.64% vs. 79.81%, p = 0.039). CONCLUSIONS:NPSS integrates MI, WSI, and 3DNP to enable accurate and efficient NP subtype diagnosis and prognosis prediction, greatly enhancing diagnostic precision and clinical utility.

Allergic diseases are common chronic inflammatory conditions, which can affect multiple organs in severe cases, resulting in complex and varied clinical manifestations. Therefore, their management requires a more comprehensive and long-term strategy. A well-balanced diet is crucial in this context, as it regulates the immune system and improves atopic constitution, making it a key measure in preventing and controlling allergic diseases. Unlike observational studies prone to confounding and reverse causality, Mendelian randomization uses genetic variants as instrumental variables for stronger causal inference. This study employed the two-sample Mendelian randomization to investigate the potential causal relationships between 22 dietary factors and allergic diseases. The primary methods used were the weighted median method, MR-Egger regression, and inverse-variance weighted. To ensure the robustness and accuracy of the results, a series of sensitivity analyses, heterogeneity tests, and pleiotropy assessments were conducted. The study identified 7 dietary factors associated with allergic asthma, atopic dermatitis, and allergic rhinitis. The oily fish (OR: 0.666; 95% CI: 0.468-0.949; P = .024), dried fruit (OR: 0.463; 95% CI: 0.307-0.697; P = .00023), and cereal intake (OR: 0.595; 95% CI: 0.355-0.998; P = .049) was found to have a protective effect against asthma. The fresh fruit (OR: 0.592; 95% CI: 0.384-0.913; P = .018), tea (OR: 0.774; 95% CI: 0.603-0.995; P = .046), cereal (OR: 0.635; 95% CI: 0.430-0.939; P = .023), and processed meat intake (OR: 0.481; 95% CI: 0.294-0.787; P = .0036) were protective factors against atopic dermatitis. No significant causal relationships were observed between other dietary factors and these 3 diseases. These findings underscore the critical role of a balanced diet in the prevention and management of allergic diseases and highlight the potential of nutritional interventions in the future control and treatment of these conditions.

BACKGROUND:Dupilumab has shown efficacy in patients with uncontrolled CRSwNP in clinical trials and real-world practice, but data in Chinese patients are limited. This study investigated the efficacy and safety of dupilumab in Chinese patients with severe CRSwNP who were not controlled on standard of care. METHODS:This placebo-controlled, Phase III trial randomized patients 1:1 to dupilumab 300 mg every 2 weeks or matching placebo for 24 weeks as add-on treatment with daily intranasal corticosteroids. The primary efficacy endpoint was change from baseline in nasal polyp score (NPS) at week 24. Patient-reported outcomes and safety were also assessed. RESULTS:63 patients were randomized (dupilumab n = 31, placebo n = 32). Baseline characteristics were well balanced between the groups. Improvement in NPS at week 24 was significantly greater with dupilumab than placebo (least square mean difference [LSMD] -1.84 [95% CI -2.53, -1.15], p < 0.0001). Dupilumab also improved patient-reported outcomes vs. placebo: nasal congestion score (LSMD -0.54 [95% CI -0.97, -0.12], p = 0.0126); total symptom score (-1.68 [-2.67, -0.69], p = 0.0008); loss of smell score (-0.62 [-1.08, -0.17], p = 0.0072); and health-related quality of life (22-item sino-nasal outcome test score) (-9.52 [-16.81, -2.24], p = 0.0104). The incidence of treatment-emergent adverse events was similar between the groups. CONCLUSIONS:Dupilumab is efficacious in Chinese patients with CRSwNP, with tolerability consistent with the known safety profile. These results support the benefits of dupilumab in Chinese patients with severe CRSwNP who are uncontrolled on standard of care therapy. TRIAL REGISTRATION:ClinicalTrials.gov identifier: NCT05878093.

Objective:To identify reliable anatomical landmarks through endoscopic dissection of the palatovaginal canal（PVC） and to introduce a novel posterior nasal neurectomy（PNN） approach via this canal, while evaluating its clinical efficacy in allergic rhinitis（AR）. Methods:Surgical-route dissection was performed on 10 dry skulls and 2 fresh cadaveric heads to obtain high-definition images of the PVC region. A retrospective analysis was conducted on 30 AR patients who underwent PNN in which the PVC served as the key landmark. Symptom severity was assessed with a visual analogue scale（VAS） pre-operatively and 12 months post-operatively. Results:Critical landmarks for the new approach were identified, including the sphenoidal process of the palatine bone, posterior aperture of the PVC, posterior sulcus, PVC itself, vomerovaginal canal, vaginal process, and sphenopalatine foramen. One year after surgery, mean VAS scores for nasal obstruction, itching, sneezing, rhinorrhea, and overall discomfort were all lower than baseline with statistically significant differences. Aside from transient palatal numbness in five patients, no other complications occurred. Conclusion:Endoscopic PNN via the palatovaginal canal is a safe and effective surgical method for the treatment of allergic rhinitis.

BackgroundHereditary vestibular dysfunctions (HVDs) are a group of diseases caused by genetic mutations, characterized by congenital or progressive vestibular dysfunction, often accompanied by hearing loss or other systemic damages. These diseases are divided into syndromic (e.g., Usher syndrome, CHARGE syndrome) and non-syndromic types, involving mutations in key genes such as MYO7A, COCH, SLC26A4, TMC1, etc. Although clinical phenotypes vary, the pathogenesis is complex, traditional diagnostic methods are limited, and effective treatments are lacking. Mouse models are important tools for studying hereditary vestibular dysfunction, providing critical platforms for understanding disease mechanisms, developing diagnostic biomarkers, and treatment strategies.MethodsThis review systematically searched English and Chinese literature in databases including PubMed, Web of Science, Embase, and CNKI from January 2000 to April 2026. The search strategy combined Medical Subject Headings (MeSH) terms and free-text keywords, including "hereditary vestibular dysfunction," "mouse models," "gene therapy," "CRISPR-Cas9," "Usher syndrome," "translational research," "biomarkers," "Meniere disease," and "International Mouse Phenotyping Consortium." Inclusion criteria were: (1) peer-reviewed articles on hereditary vestibular dysfunction mouse models; (2) studies reporting genetic mechanisms, pathophysiology, or therapeutic interventions; and (3) English or Chinese language publications. Exclusion criteria were: (1) non-peer-reviewed conference abstracts or preprints and (2) studies without clear genetic or phenotypic characterization. Two authors independently screened titles, abstracts, and full texts, with disagreements resolved by consensus. The review focuses on analyzing the applications of spontaneous mutation models, genetic engineering models, CRISPR technology-based models, and knockout models from the International Mouse Phenotype Consortium (IMPC) in disease mechanism research and treatment development.ResultsIn recent years, significant progress has been made in hereditary vestibular dysfunction mouse model research. Spontaneous mutation models like Myo6 and Cdh23 mutant mice have revealed the key role of cytoskeletal and cell junctions in vestibular function. Genetic engineering models have successfully simulated a variety of diseases, including Usher syndrome, ion channel defects, and vestibular development abnormalities, elucidating the molecular mechanisms of TMC1/2 mechanosensory channels, SLC26A4 ion transport, and vestibular system development genes. The application of CRISPR-Cas9 technology has greatly improved model construction efficiency and precision. These models have shown positive results in gene therapy, gene editing, and drug treatment research. AAV-mediated gene replacement therapy, CRISPR gene repair, and new drugs such as α1-antitrypsin have all achieved positive outcomes in mouse models. Biomarker studies based on multi-omics techniques have identified potential diagnostic markers such as Slc17a6 and BDNF.ConclusionMouse models play an irreplaceable role in the study of hereditary vestibular dysfunction, providing a solid foundation for elucidating disease mechanisms, improving diagnostic methods, and developing treatment strategies. Although clinical translation still faces challenges such as species differences, delivery efficiency, and treatment windows, with the continuous development of gene editing technology, nano-delivery systems, and multi-omics techniques, personalized diagnosis and treatment for hereditary vestibular dysfunction are expected to be realized, bringing new hope to patients.

Restoring CD8⁺T cell infiltration and potentiating anti-tumor immune responses in the tumor microenvironment (TME) is critical for developing effective immunotherapies against triple-negative breast cancer(TNBC), while the regulatory role of N⁶-methyladenosine (m⁶A)-modified circular RNAs (circRNAs) in TNBC immune escape remains largely unelucidated. Whole-transcriptome microarray analysis combined with bioinformatics mining was conducted on TNBC tissues to screen circRNAs associated with immune evasion. RNA immunoprecipitation (RIP), RNA pulldown, and methylated RNA immunoprecipitation (MeRIP) assays were performed to verify the m⁶A modification of circFOXA1 and its interaction with gasdermin C (GSDMC). In vitro T cell-mediated tumor cytotoxicity assays and in vivo xenograft models in C57BL/6 mice were used to investigate the functional roles of the circFOXA1/GSDMC axis in TNBC anti-tumor immunity. Luciferase reporter and actinomycin D assays were further applied to clarify the regulatory mechanism of GSDMC on OTUB1 and programmed cell death-ligand 1 (PD-L1) expression. CircFOXA1 was identified as an m⁶A-modified circRNA with high stability and upregulation in TNBC, and its expression was significantly negatively correlated with CD8⁺T cell infiltration in TNBC tissues. Functionally, circFOXA1 induced immunosuppression in a CD8⁺T cell-dependent manner both in vitro and in vivo. Mechanistically, the m⁶A writer METTL14 mediated the m⁶A modification of circFOXA1, and the m⁶A reader YTHDF2 promoted circFOXA1 circularization. CircFOXA1 impaired immune cell-dependent tumor killing by upregulating GSDMC expression, which further enhanced OTUB1 mRNA stability at the post-transcriptional level. OTUB1-mediated deubiquitination subsequently stabilized PD-L1 protein, ultimately inhibiting CD8⁺T cell infiltration and driving TNBC immune escape. This study identifies a novel regulatory axis of m⁶A-modified circFOXA1/GSDMC/OTUB1/PD-L1 in mediating TNBC immune escape, where GSDMC enhances PD-L1 protein stability via OTUB1-dependent deubiquitination. These findings reveal a new molecular mechanism underlying TNBC immune evasion and identify circFOXA1 as a potential therapeutic target to improve the efficacy of anti-PD-1/PD-L1 immunotherapy in TNBC.

Background: Patients with moderate-to-severe allergic rhinitis (AR) often experience a heavy clinical burden and require more medications to alleviate nasal symptoms. The aim of this study was to evaluate the efficacy and safety of GSP301, a fixed-dose combination nasal spray containing olopatadine hydrochloride and mometasone furoate, in patients with seasonal AR (SAR). Methods: In this multicenter, randomized, double-blind, parallel-group study, moderate-to-severe SAR patients were assigned at a 1:1:1 ratio to receive intranasal GSP301, olopatadine hydrochloride (OLO), or mometasone furoate (MF) for 14 days. The primary endpoint was the change from baseline in the average A.M. and P.M. 12-hour reflective total nasal symptom score (rTNSS). Secondary endpoints included changes in the instantaneous TNSS (iTNSS), individual nasal symptoms, reflective total ocular symptom score (rTOSS), instantaneous total ocular symptom score (iTOSS), individual ocular symptoms, and rhinoconjunctivitis quality-of-life questionnaire (RQLQ). Exploratory endpoints and adverse events were also analyzed. Results: Among the 534 subjects, the GSP301 group demonstrated statistically significant improvements in the average rTNSS compared with the OLO group [posterior least square mean difference (LSMD) =-0.56; P < 0.0001] and the MF group (posterior LSMD =-0.43; P < 0.0001). Consistent benefits were observed across secondary endpoints, including iTNSS, rTOSS, RQLQ, and individual nasal and ocular symptoms (all P < 0.05). Additionally, GSP301 reduced the levels of interleukin (IL)-5 and eosinophilic cationic protein (ECP) in nasal secretions. Treatment-emergent adverse events (TEAEs) occurred in 11.2%, 13.5%, and 11.3% of patients in the GSP301, OLO, and MF groups, respectively. Conclusion: Compared with OLO and MF, GSP301 demonstrated superior efficacy, safety, and potential advantages in alleviating local inflammation in patients with moderate-to-severe SAR.

The prevalence of allergic rhinitis (AR) continues to rise, severely impairing patients’ quality of life and causing enormous social and economic burdens. For refractory AR that cannot be adequately controlled by standardized firstline therapies, neurotomy has become an important secondline therapeutic option. However, due to various remaining controversial issues, there is currently a lack of internationally unified clinical guidelines, which restricts its clinical application and generalization. To better guide the clinical practice of neurotomy for AR in China, 49 experts in the field of rhinology and allergy nationwide, led by the Third Affiliated Hospital of Sun Yat-sen University, carried out the work of formulating a consensus. Using the Delphi method, we focused on seven dimensions: the purpose and significance of neurotomy for AR, relevant applied anatomy, pathophysiological basis, surgical indications and contraindications, surgical techniques, efficacy and evaluation criteria, and surgical complications and their management, ultimately generating a series of core viewpoints. This consensus is expected to further promote the standardized development of neurotomy for AR in China, and help improve the overall prevention and management of AR.

PURPOSE:Allergic rhinitis (AR) is no longer considered an immune dysregulation disorder but rather a neuroimmune disorder regulated by neuronal signals. However, the mechanisms underlying these effects remain unclear. Therefore, we evaluated whether the local nasal mucosa is regulated by neuroimmune signals during nasal allergic reactions. METHODS:We identified genes that were differentially expressed between patients with AR and healthy controls using GSE46171 gene chip data. Expression levels of neuromedin U (NMU), NMU receptor 1 (NMUR1), and group 2 innate lymphoid cells (ILC2s) in the nasal mucosa were determined the impacts of NMU on patients with AR were assessed. An AR animal model was established to observe the effects of local NMU intervention on local and systemic ILC2s in the nasal cavity. RESULTS:We identified 1,137 differentially expressed genes and focused on the neuropeptide NMU. NMU was widely distributed in the lamina propria of the nasal mucosa of patients with AR. NMUR1 was expressed at high levels in the lamina propria, basal layer, and glandular epithelium. Local ILC2 expression in the nasal mucosa of the AR group was elevated and positively correlated with NMU and NMUR1 expression. Using the AR model, we found that NMU significantly enhanced both local and systemic inflammatory responses in ovalbumin-sensitized mice and promoted activation of ILC2s to release additional type 2 inflammatory cytokines. However, this effect was blocked by an extracellular signal-regulated kinase (ERK) pathway inhibitor, indicating that NMU activates ILC2s via the ERK pathway, contributing to AR pathogenesis. CONCLUSIONS:During nasal allergic reactions, local NMU increases significantly in the nasal cavity, activating ILC2s via the ERK pathway to release type 2 cytokines, thereby participating in or exacerbating the onset of AR. These findings lay the groundwork for exploration of diverse factors that contribute to AR and suggest new approaches to prevention and treatment.

BACKGROUND:Chronic rhinosinusitis (CRS) leads to a burden in life and economy. Better therapies need to be explored. OBJECTIVE:This stage I study aims to explore the efficacy and safety of intranasal corticosteroids combined with mucoactive drugs for CRS. METHODS:This randomized-controlled, double-blind study was conducted at 13 hospitals from 2021.01.31 to 2023.01.17. CRS patients were randomly assigned into the eucalyptol-limonene-pinene enteric capsules (ELP) group or placebo group, both using budesonide nasal spray (two doses of 64 μg into each nostril twice a day), and followed up at baseline, week 4, and week 8. The difference of Major Symptom Score (MSS) sum score from baseline to week 8 was defined as the primary endpoint. RESULTS:The data of 291 patients (ELP group: 146 VS. placebo group: 145) were analyzed. The improved mean (SD) of MSS of the budesonide-ELP patients was 4.24 (2.59) at week 4 and 4.37(2.64) at week 8, higher than 3.51(2.27) (Pweek 4 = 0.012) and 3.85 (2.47) (Pweek 8 = 0.093) of budesonide-treated patients, respectively. While, the budesonide-ELP patients had a higher improvement percentage in nasal congestion, postnasal drip, rhinorrhea, and anosmia at week 8 (all P < 0.05). The current clinical control questionnaire in the ELP group significantly differed with placebo group patients at week 4 (P = 0.012), but not at week 8 (P = 0.681). Moreover, the change of Lund-Mackay (LM) and VAS between the two groups was not different at week 8, respectively. However, the CT score of budesonide-ELP-treated patients has significantly improved among smokers at week 8 (P = 0.022). CONCLUSION:Intranasal corticosteroid combined with mucoactive drugs therapy (budesonide-256 μg/day combined with ELP enteric capsules-0.8 g/day) has the potential to improve subjective symptoms and promote physiological recovery for adult patients with CRS, especially for smokers.

Mounier–Kuhn syndrome (MKS) is characterized by tracheobronchomegaly with thinning or atrophy of the elastic tissue. Due to low clinical awareness, MKS is frequently overlooked on chest CT examinations, leading to diagnostic delays. This study aimed to synthesize the historical context and contemporary advancements in MKS research. Five MKS cases were retrospectively identified through thoracic imaging review at our institution. A systematic review adhering to PRISMA guidelines was conducted across Web of Science (WOS) and China-specific databases (China National Knowledge Infrastructure [CNKI], Wanfang) from January 2000 to March 2025 to identify studies reporting CT-confirmed tracheobronchial dilation, to address geographic bias. Concurrently, a bibliometric analysis of WOS publications spanning January 1962 to March 2025 was performed using predefined inclusion criteria to analyze historical research trends through VOSviewer. Our institutional cohort (5 patients: 4 males) exhibited marked tracheobronchial dilation, with two representative cases demonstrating distinct clinical trajectories of disease progression. Systematic analysis of 147 publications encompassing 169 radiologically confirmed cases revealed significant male predominance (male-to-female ratio: 5.5:1), a mean tracheal diameter of 34.3 ± 6.1 mm, a median diagnostic delay of 3.0 years (IQR: 0.25–20.0 years), and high comorbidity prevalence including bronchiectasis (71.6

Allergic rhinitis (AR) is a common disease in preschool children and seriously affects their quality of life. Defining the risk factors of AR can help early diagnosis and prevention. The aim of this meta-analysis was to identify and summarizes the risk factors associated with allergic rhinitis in preschool children. A systematic search of PubMed, Embase, Cochrane library, Web of Science, built up to 20 January 2025 was performed. Studies were included if they reported risk factors for AR in preschool children. A random-effects model was used to calculate the combined odd ratio (OR) and 95

Background:MP-AzeFlu (Dymista; Meda Pharma GmbH & Co., KG), a formulation combining azelastine hydrochloride and fluticasone propionate in a single spray, is superior to fluticasone propionate alone in relieving symptoms and improving the quality of life of patients with allergic rhinitis.Objectives:In this study, we evaluated whether the effect of AzeFlu, a generic drug manufactured from China, is equivalent to that of MP-AzeFlu.Methods:In total, 679 patients were recruited for a multicentre, randomized, double-blind, original drug-controlled, and parallel-group clinical trial. Overall, 339 and 340 patients were administered with AzeFlu and MP-AzeFlu, respectively. Efficacy was assessed by changes in the reflective total nasal symptom score, the area under the curve of reflective total nasal symptom score changes over time, changes from baseline in individual nasal symptom scores, and the Rhinoconjunctivitis Quality of Life Questionnaire. In addition, a safety evaluation was simultaneously performed.Results:AzeFlu and MP-AzeFlu reduced the reflective total nasal symptom score from baseline (AzeFlu -6.7 [standard deviation, 2.59]; MP-AzeFlu -6.7 [standard deviation, 2.76]; P = 0.905) and improved nasal symptoms and quality of life (AzeFlu -62.3 [standard deviation, 33.59]; MP-AzeFlu -64.7 [standard deviation, 33.73]; P = 0.394) in patients with allergic rhinitis. Significant differences were not observed between groups.Conclusion:AzeFlu showed effects equivalent to those of MP-AzeFlu in this clinical trial and may benefit Chinese patients with allergic rhinitis.Registration number: CTR20190189 (chinadrugtrials.org.cn/index.html)Conclusion:AzeFlu showed effects equivalent to those of MP-AzeFlu in this clinical trial and may benefit Chinese patients with allergic rhinitis.Registration number: CTR20190189 (chinadrugtrials.org.cn/index.html)

Goblet cell hypersecretion is a hallmark of airway inflammation and is driven by complex neuroimmune regulation involving submucosal glands and goblet cells. Although studies have focused on mast cell degranulation as a critical driver of nasal secretion, the role of goblet cells in this process is relatively under-researched. In allergic airway inflammation, goblet cells exhibit metaplasia and hypersecretion. However, allergen exposure does not directly trigger goblet cell degranulation, raising questions regarding the underlying mechanisms of these reactions. The activation of enteric neurons promotes goblet cell degranulation by stimulating the calcitonin gene-related peptide (CGRP)–receptor active modification protein-1 (RAMP1) axis. Meanwhile, airway goblet cells express various neuropeptide receptors, and their activation by neuropeptides such as substance P and CGRP induces mucus secretion, exacerbating allergic rhinitis-associated hypersecretion. Thus, although previously less recognised, the neuron–goblet cell signalling axis plays a critical role in allergic rhinitis mucus secretion. This review highlights current research on the neuroimmune mechanisms underlying goblet cell metaplasia and degranulation, focusing on allergic rhinitis, so as to guide clinical treatment strategies.

OBJECTIVES:Nasal epithelial cells initiate innate responses to allergens by releasing IL-1 family cytokines, such as IL-33, and disrupting the mucosal barrier. TRPV1 has gained increasing recognition for its role in immune modulation in allergic conditions. This study aimed to elucidate the mechanisms by which epithelial cells detect allergens and explore the pivotal role of TRPV1 in regulating innate nasal epithelial responses. METHODS:To identify TRPV1-related genes and pathways, the GSE167225 dataset was analyzed. To validate TRPV1 expression, clinical data and nasal tissues from 34 patients with AR and 13 controls were collected. To further investigate its mechanisms, OVA-sensitized C57BL/6 mice were exposed to the TRPV1 antagonist SB-705498, and TRPV1 knockout mice were utilized. Primary human nasal epithelial cells were used for in vitro experiments, and various assays, including reverse transcription polymerase chain reaction(RT-PCR), western blotting(WB), and others, were performed to assess gene expression and signaling pathways. RESULTS:Bioinformatics and clinical analysis revealed elevated TRPV1 expression in patients with AR, positively correlated with nasal itching and sneezing severity(R = 0.6493, P < 0.001; R = 0.4906, P < 0.001). In vivo, SB-705498 and TRPV1 ablation significantly alleviated allergy symptoms, reduced allergen-induced IL-33 release, and prevented disruption of tight junction protein occludin in murine models. In vitro, TRPV1 antagonism suppressed capsaicin-induced calcium influx, NF-κB activation, and IL-33 overexpression. CONCLUSIONS:Allergen exposure enhances the secretion of IL-33 in hNECs via the TRPV1-NF-κB pathway, thus compromising epithelial tight junction integrity. Inhibition of TRPV1 can attenuate the effects of allergen-induced innate nasal epithelial responses. Our study offers novel insights into the potential therapeutic targeting of TRPV1 in AR.

Aim:This study aimed to systematically analyze the neuro-regulation mechanisms of airway hyperreactivity disease using bibliometrics, focusing on the research status and progress of two key regulatory networks: the "lung-brain axis" and the "nasal-brain axis", to further characterize the "nasal-brain axis". Methods:A bibliometric analysis of 626 articles published between 1991 and 2024 was conducted to assess the growing interest in the impact of neuro-immune mechanisms and psychological stress on airway diseases, including asthma and allergic rhinitis (AR). Results:The study findings revealed that interactions between neuro-immune signaling pathways and the central nervous system are crucial for understanding airway hyperreactivity, with the United States leading research contributions. Key themes identified in this study include allergic asthma, neuroinflammation, and the lung-brain axis, revealing bidirectional communication pathways between peripheral and central immune responses. Conclusion:Based on studies of asthma and the lung-brain axis, we anticipate that AR and the nasal-brain axis likely involve similar neuro-immune mechanisms and peripheral-central response circuits. The nasal-brain axis theory was further supported by its integration with the unified airway hypothesis, solidifying its role as a crucial regulatory mechanism in airway inflammation research.

Objective:Inflammation has been confirmed to play an important role in the occurrence and development of sudden sensorineural hearing loss（SSNHL）, and the neutrophil-to-lymphocyte ratio（NLR） is a biomarker positively correlated with the degree of inflammation. This study aims to identify the difference in serum NLR between patients with SSNHL and normal population, and to evaluate the predictive efficacy of NLR for the occurrence and prognosis of SSNHL, thereby guiding the clinical diagnosis and treatment of SSNHL. Methods:In this study, 96 patients diagnosed with SSNHL admitted to our department from January 2023 to March 2024 and 96 patients diagnosed with vocal cord polyps admitted to our department during the same period were recruited as a control group. Multivariate Logistic regression was used to evaluate independent related factors, and a nomogram was constructed to predict the probability of SSNHL. The receiver operating characteristic（ROC） curve and calibration curve were used to evaluate the accuracy of prediction. Results:Multivariate logistic regression analysis showed that a high level NLR（OR2.215; 95%CI1.597-3.073; P<0.001） were independently associated with the presence of SSNHL. High age（OR1.036; 95%CI1.009-1.067; P=0.012）, high FIB（OR2.35; 95%CI1.176-4.960; P=0.019） were the risk factor for SSNHL. Incorporating these 3 factors, a forest plot and a nomogram were generated. The ROC curve, nomogram and calibration curve showed that the model had good clinical practicability. A low NLR（OR0.598; 95%CI0.439-0.816; P<0.001） was significantly associated with a favorable prognosis of SSNHL. Conclusion:Elevated NLR can serve as an promising biomarker for assessing the risk of SSNHL. The nomograms calculation model may be utilized as a tool to estimate the probability of SSNHL. Low level NLR is significantly associated with a good prognosis of SSNHL.

Introduction: The objective of the present study was to evaluate the efficacy and safety of MP-AzeFlu nasal spray in comparison to commercially available azelastine hydrochloride and fluticasone propionate sprays in Chinese patients with moderate-to-severe allergic rhinitis (AR).Methods: We conducted a 14-day multicenter, randomized, double-blind, active controlled prospective clinical study in adult and adolescent patients with AR, who had moderate-to-severe symptoms. The primary efficacy endpoint was the change from baseline in combined 12-h reflective total nasal symptom score (rTNSS) (morning [AM] + afternoon [PM]). The safety profile of the study medications was assessed through the recording, reporting, and analysis of baseline medical conditions, adverse events (AEs), vital signs, and focused nasal examination. Three hundred patients per treatment group were randomized, which led to a total sample size estimation of 900 patients.Results: MP-AzeFlu group showed significantly higher symptom reduction for the entire 2-week treatment period in rTNSS when compared with the AZE group (LS mean difference: - 1.96; 95% CI: - 2.53, - 1.39; p < 0.0001), or the FLU group (LS mean difference: - 0.98; 95% CI: - 1.55, - 0.41; p = 0.0007). The results of adult RQLQ showed improvement in QoL in all treatment groups. Except for dysgeusia (bitter taste) that was reported by more patients (13 [4.3%]) in the MP-AzeFlu group, the incidence of all other TEAEs in the MP-AzeFlu group was comparable or even lower than in other treatment groups.Conclusions: MP-AzeFlu, when administered as one spray per nostril twice daily for 14 days, alleviated AR symptoms in Chinese patients with moderate-to-severe AR.

CD46 can facilitate the production of IgE. Activation of CD46 may contribute to the pathogenesis of allergic diseases. The aim of this study is to elucidate the association between CD46 expression in B cells and the pathogenesis of airway allergy. In this study, peripheral B cells were collected from a group of patients suffering from allergic rhinitis (AR). An AR mouse model was established to test the role of CD46 in the development of airway allergy. The results showed elevated amounts of IGE in peripheral CD46+ B cells of AR patients. CD46+ B cells of AR patients showed high reticulum endoplasmic (ER) stress status. The expression of CD46 in peripheral B cells was positively associated with the AR response in patients. The production of IgE in mice with airway allergy was prevented by ablating CD46 expression in B cells. Exposure to aluminum hydroxide up regulated the expression of Cd46 in B cells through exacerbating ER stress. Administration of Cd46 shRNA carrying nanoparticles attenuated experimental airway allergy. In conclusion, peripheral B cells in AR patients display elevated CD46 expression. Cd46 ablation in B cells can mitigate the production of IgE in mice and attenuate experimental airway allergy.