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Journal articleWang M, He Y, Hu H, et al., 2026,
Protective role of fatty acid oxidation against epithelial barrier dysfunction in allergic asthma.
, Redox Rep, Vol: 31BACKGROUND: Fatty acid oxidation (FAO) is implicated in lung diseases, but its role in bronchial asthma is not fully understood. We investigated its effect on airway epithelial barrier integrity. METHODS: Using a house dust mite (HDM)-induced murine asthma model and HDM, IL-4, IL-13, or TNF-α stimulated human primary bronchial epithelial cells (BECs) and bronchial epithelial (Beas-2b) cells, we modulated FAO with L-carnitine (agonist) and Etomoxir (inhibitor). BECs and Beas-2b cells were infected with lentivirus-mediated CPT1A shRNA prior to stimulation. Barrier function, mitochondrial oxidative stress, inflammation, and metabolism were assessed. RESULTS: FAO level in lungs negatively correlated with increased inflammation and tissue injury in HDM-induced asthmatic mice (all p < 0.05), while positively regulating tight junction protein expression. In BECs and Beas-2b cells, Etomoxir treatment and CPT1A knockdown exacerbated the impairment of FAO caused by various stimulants (all p < 0.05). Furthermore, FAO negatively regulated HDM/cytokine-induced epithelial barrier damage, hyperactive inflammatory response, and mitochondrial dysfunction in Beas-2b cells (all p < 0.05). In contrast, treatment with L-carnitine significantly alleviated these pathophysiological features in both in vivo and in vitro models. CONCLUSION: FAO plays a protective role in the occurrence and development of asthma by maintaining airway epithelial cell homeostasis and barrier function.
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Journal articleHasegawa T, Yang F, Kermani N, et al., 2026,
Sputum eosinophil and neutrophil activation biomarkers in severe asthma
, ERJ Open Research, Pages: 00602-2026<jats:sec> <jats:title>Background</jats:title> <jats:p>Asthma is characterized by different inflammatory phenotypes. We hypothesized that sputum eosinophil-derived neurotoxin (EDN), and myeloperoxidase (MPO) or interleukin-8 (IL-8) levels improves the granulocytic characterization of asthma compared to sputum granulocyte counts.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods</jats:title> <jats:p>EDN, IL-8 and MPO were assayed in induced sputum supernatants from patients with severe and mild-to-moderate asthma, and healthy controls. Elevated cut-off values were determined using Youden Index. Asthma patients were stratified in four subgroups based on EDN and IL8 or MPO levels.</jats:p> </jats:sec> <jats:sec> <jats:title>Results</jats:title> <jats:p> Sputum EDN, IL-8 and MPO levels were higher in severe asthma (n=193) than in controls (n=40). Optimal cut-offs were 103.5 ng·mL <jats:sup>−1</jats:sup> for EDN, 1150.7 pg·mL <jats:sup>−1</jats:sup> for IL-8 and 220 ng·mL <jats:sup>−1</jats:sup> for MPO. 53 patients (23%) were EDN <jats:sup>High</jats:sup> IL-8 <jats:sup>Low</jats:sup> , 16 (7%) EDN <jats:sup>Low</jats:sup> IL-8 <jats:sup>High</jats:sup> , 112 (49%) EDN <jats:sup>High</jats:sup> IL-8
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Journal articleHine J, Bush A, De Simoni A, et al., 2026,
Financial INcentives to improve Asthma (FINA): a pilot RCT to improve medication adherence for children and young people with asthma
, Archives of Disease in Childhood, ISSN: 0003-9888<jats:sec> <jats:title>Objective</jats:title> <jats:p>To assess effectiveness and feasibility of financial incentives to improve medication adherence for children and young people (CYP) with asthma.</jats:p> </jats:sec> <jats:sec> <jats:title>Design</jats:title> <jats:p>Pilot randomised controlled trial measuring adherence in CYP using an electronic monitoring device (EMD) with twice-daily reminders; design supported by patient and public involvement.</jats:p> </jats:sec> <jats:sec> <jats:title>Setting</jats:title> <jats:p>CYP were recruited between 2 and 12 weeks after attendance at an emergency department (ED) following a severe asthma exacerbation.</jats:p> </jats:sec> <jats:sec> <jats:title>Patients</jats:title> <jats:p>CYP aged 11–17 years old with asthma, who were prescribed inhaled corticosteroids for at least 6 months prior to their exacerbation, owned their own smartphone and understood verbal and written English.</jats:p> </jats:sec> <jats:sec> <jats:title>Interventions</jats:title> <jats:p>Intervention CYP received £1 per complete morning/£1 per complete evening inhaler dose(s) for 12 weeks (max £168). Controls received usual care (with EMD and reminder use) with no financial incentives.</jats:p> </jats:sec> <jats:sec> <jats:title>Main outcome measures</jats:title> <jats:p>adherence, asthma control and psychological outcomes. F
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Journal articleHatziagorou E, Bush A, 2026,
Home spirometry in bronchiectasis: when does a measurement become medicine?
, Thorax, ISSN: 0040-6376 -
Journal articleSilva AE, Ferrante G, Silveyra P, et al., 2026,
Peripubertal changes in asthma.
, Am J Respir Crit Care Med, Vol: 212, Pages: 2592-2606Asthma is a heterogeneous disease affecting nearly 300 million people around the world. It is the most common chronic respiratory disease of childhood. There are significant sex differences in asthma incidence, severity, and morbidity around the time of puberty. The reasons for these peripubertal changes are still not fully understood, but they are likely multifactorial. In this review, we will discuss several proposed contributing mechanisms, including sex differences in anatomy and development, the effects of sex hormones on airway inflammation and reactivity, the immunomodulatory effects of sex hormones, differences in mucociliary function, and sex differences in genetic and epigenetic factors.
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Journal articleKhor YH, Luppi F, Adegunsoye A, et al., 2026,
Acute exacerbation in fibrotic interstitial lung disease: an international working group report.
, Am J Respir Crit Care Med, Vol: 212, Pages: 2358-2385Acute exacerbations (AEs) occur both in patients with idiopathic pulmonary fibrosis (IPF) and those with non-IPF fibrotic interstitial lung disease (fILD). These events confer high morbidity and mortality, with a lack of proven effective therapeutic interventions. The objective of this state-of-the-art document is to summarize latest evidence since the 2016 International Working Group Report on AE-IPF, expanding it across the spectrum of all fILDs. A comprehensive literature review on the epidemiology, associated and risk factors, prognosis, and management of AE-fILD is summarized. In addition to revising the AE definition and diagnostic criteria for broad application across different fILDs, a conceptual framework for acute respiratory worsening (ARW) has been proposed to encompass a variety of acute respiratory deteriorations, both related and unrelated to AEs. This allows structured evaluation in both clinical and research settings. The proposed revised definition for AE-fILD is an acute respiratory event characterized by increased respiratory symptoms or signs and associated with radiologic or histologic features consistent with diffuse alveolar damage (with or without superimposed organizing pneumonia) in a patient with known or newly diagnosed fILD. On the other hand, ARW refers to a heterogeneous group of clinical events with acute symptom worsening not attributable to diffuse alveolar damage in patients with fILD, such as pulmonary edema, bronchitis, and pneumonia, although severe pneumonia can trigger AE-fILD. Additionally, we discuss considerations for inclusion of AE as a clinical trial endpoint, as well as research priorities for advancing knowledge on the pathogenic mechanisms, event prediction, risk stratification, and development of drugs and supportive treatments.
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Journal articleBush A, Ramsey B, 2026,
Cystic fibrosis in 2026: game over, or game on? Introduction to an AJRCCM special section on cystic fibrosis.
, Am J Respir Crit Care Med, Vol: 212, Pages: 2518-2519 -
Journal articlePugashetti JV, Jee AS, Yu AR, et al., 2026,
Mycophenolate and azathioprine in fibrotic interstitial lung disease.
, Am J Respir Crit Care Med, Vol: 212, Pages: 2493-2503RATIONALE: Immunosuppression is routinely used for non-idiopathic pulmonary fibrosis (IPF) interstitial lung diseases (ILDs), despite limited trial evidence and unclear impact on long-term outcomes. OBJECTIVES: To evaluate whether mycophenolate or azathioprine improves 3-year transplant-free survival and lung function trajectory in fibrotic ILD, including non-IPF idiopathic interstitial pneumonia (IIP), fibrotic hypersensitivity pneumonitis (fHP), and connective tissue disease (CTD)-associated ILD. METHODS: We employed a clone-censor-weighting framework to emulate a randomized controlled trial in this multicenter retrospective study. Each patient was cloned and assigned to immunosuppression initiation within 6 months of enrollment or no initiation strategies and censored when the assigned strategy deviated from observed treatment. Stabilized inverse probability treatment and censoring weights were used. MEASUREMENTS: The primary endpoint was 3-year transplant-free survival assessed with weighted Cox models across treatment strategies. Weighted generalized estimating equations were used to model lung function trajectory. MAIN RESULTS: Among 2270 included patients, 18% (186/1022) with non-IPF IIP, 30% (162/544) with fHP, and 31% (221/704) with CTD-ILD were initiated on immunosuppression within 6 months. Immunosuppression was not associated with improved survival within any ILD subtype but was associated with worse survival in non-IPF IIP (hazard ratio [HR] = 1.38; 95% CI, 1.04-1.84) and fHP (HR = 1.62; 95% CI, 1.09-2.40). Immunosuppression was not associated with differential lung function trajectory within any ILD subtype. CONCLUSIONS: In this study, immunosuppression initiation showed no evidence of benefit for 3-year transplant-free survival or lung function and was associated with higher mortality in select fibrotic ILD subtypes. Prospective randomized controlled trials are needed to inform patient care.
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Journal articleLele S, Pillai A, Quayum M, et al., 2026,
Combined Large and Small Airway Obstruction Is Associated With Increased Exacerbation Frequency and Poorer Symptom Control in Persistent Asthma.
, J Allergy Clin Immunol Pract, Vol: 14, Pages: 2348-2355.e3BACKGROUND: Spirometry remains central to the assessment of asthma but may fail to detect small airways dysfunction (SAD), which contributes to considerable symptoms and exacerbation risk. OBJECTIVE: We investigated whether integrating oscillometry with spirometry improves physiological phenotyping and risk stratification in asthma. METHODS: In this retrospective, multicenter study, data from 1497 adults with asthma were analyzed from the Oscillometry Asthma Registry. SAD was defined using the ratio of resistance heterogeneity between 5 and 20 Hz to resistance at 5 Hz ≥19% and airflow obstruction as forced expiratory volume in 1 second/forced vital capacity (FEV1/FVC) <70%. Participants were categorized into 4 mutually exclusive groups: (1) group 1-normal oscillometry and normal spirometry, (2) group 2-abnormal oscillometry with normal spirometry, (3) group 3-normal oscillometry with abnormal spirometry, and (4) group 4-abnormal oscillometry and abnormal spirometry. Associations with symptom control, exacerbations, and type 2 inflammatory biomarkers were assessed using multivariable logistic regression. RESULTS: For ≥1 exacerbation, the adjusted odds ratios (aORs) (95% confidence intervals) for group 4 were as follows: versus group 1, 3.19 (2.31, 4.42); versus group 2, 1.99 (1.46, 2.74); and versus group 3, 1.59 (1.07, 2.37). Corresponding aOR values for group 3 were as follows: versus group 2, 1.26 (0.85, 1.86), and versus group 1, 2.01 (1.37, 2.94). The aOR for ≥1 exacerbation for group 2 versus group 1 was 1.60 (1.18, 2.16). Results were similar when using FEV1/FVC <lower limit of normal instead of traditional predicted values. CONCLUSIONS: The combined use of oscillometry and spirometry identifies distinct physiological phenotypes of asthma with clinically meaningful differences in symptom burden and exacerbation risk.
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Journal articleYang F, Marshall DC, Howell I, et al., 2026,
Exacerbation trajectories in biologic-eligible severe asthma patients
, CHEST, ISSN: 0012-3692 -
Journal articleVassileva SM, Khamas SS, Dyhre-Petersen N, et al., 2026,
The impact of benralizumab and dupilumab on exhaled volatile organic compound profiles of severe asthma patients - a preliminary analysis.
, Respir Med, Vol: 262Volatile organic compounds (VOCs) in exhaled breath reflect biological processes in the lungs. Exploring VOC profiles in severe asthma patients starting biologics may reveal treatment-related biological changes over time. This study aimed to assess the performance and feasibility of applying a sparse partial least squares-discriminant analysis (sPLS-DA) analytical approach in detecting longitudinal changes in exhaled VOCs of patients with severe asthma initiating biologic treatment. Exhaled breath was collected in the 3 TR-ABC study, a multicenter observational prospective cohort study, at baseline and 4 months after starting biologics (benralizumab or dupilumab). VOCs were trapped on thermal desorption tubes and analyzed by gas chromatography-mass spectrometry. Paired sPLS-DA was used to distinguish baseline from post-treatment VOC profiles, and Kendall rank correlation assessed associations with clinical parameters at baseline. Data from two sites (Amsterdam and Copenhagen) were available of 25 severe asthma patients. The sPLS-DA resulted in a model containing five VOCs (methyl isobutyl ketone, 2-ethyl-1-hexanol, 5-methyl octadecane, 2-methylundecane and 1,1'-oxybis(decane)) with an area under the receiver operating characteristic curve of 0.89 (95% confidence interval: 0.79-0.99) for distinguishing baseline and 4 months post treatment. At baseline, a positive correlation was observed between 2-ethyl-1-hexanol and asthma control (Asthma Control Questionnaire); τ = 0.40, p < 0.01. A negative correlation was found between 1,1'- oxybis(decane) and blood eosinophil counts (τ = -0.30, p = 0.04). Based on our results, the proposed analytical approach appears feasible for analyzing longitudinal data in patients with severe asthma initiating biologics. Further validation in larger cohorts is warranted to confirm robustness and generalizability.
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Journal articleBush A, 2026,
Update in childhood asthma.
, Allergol Int, Vol: 75, Pages: 511-520The areas covered represent a personal selection in the field. Asthma is defined in this manuscript as a clinical syndrome of wheeze, breathlessness and chest tightness, sometimes with excess cough. No assumptions are made about underlying pathology, and asthma thus becomes a clinical description, not a diagnosis. The areas covered include the need never to forget the importance of getting the basics right, including correct diagnosis and appropriate management; most children with asthma do not need biologics. Recent advances in preschool wheeze are covered next, especially the beginnings of phenotype-driven treatment, and the difficult issue of understanding non-eosinophilic wheezing. It is becoming clearer that infection likely plays a big role, but management is very difficult with no evidence base. We are now coming to realize the importance of phenotyping acute asthma attacks; one size does not fit all, but whereas many are eosinophilic, some are infection driven and are non-eosinophilic, especially in the preschool years. A phenotypic approach may allow us to reduce the burden of repeated oral corticosteroid bursts. Furthermore, we need to move beyond mere cell counting to assessing functional status. We are increasingly appreciating the importance of replacing short-acting β-2 agonist reliever therapy with combined inhaled corticosteroid and a fast acting short- and especially long-acting β-2 agonists. Finally, the use of biologicals in severe asthma is discussed. The possibility that early use of biologics may induce remission or even cure asthma.
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Journal articleGuan WJ, Chalmers JD, Sun YC, et al., 2026,
Identification and treatment of GOLD stages I and II chronic obstructive pulmonary disease
, Journal of Thoracic Disease, Vol: 18, ISSN: 2072-1439- Cite
- Citations: 1
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Journal articleTorres MJ, Shamji MH, Arasi S, et al., 2026,
The EAACI Declaration of Salamanca: A European Roadmap for Strengthening Undergraduate Medical Education in Allergy and Clinical Immunology.
, AllergyAllergic diseases are among the most prevalent chronic conditions in Europe, yet undergraduate medical curricula lack structured Allergy and Clinical Immunology (ACI) teaching. Moreover, desite advances in specialist education, postgraduate university training varies due to differences in specialty recognition, regulatory frameworks, and the implementation of the European Training Requirements. These disparities contribute to inconsistent physician competencies, limited academic visibility of the specialty, and unequal access to high-quality allergy care. This Position Paper, developed within the framework of the Declaration of Salamanca, analyses the current educational landscape, identifies the main barriers to integrating ACI into medical education, and proposes a strategic roadmap for future development. Evidence from an EAACI-led European survey, published studies, and expert consensus demonstrates substantial variability in undergraduate curricula, limited academic representation of allergists, fragmented integration of basic immunology and clinical allergy, and challenges in educational innovation, including digital learning and artificial intelligence. The Declaration of Salamanca advocates a coordinated European strategy focused on strengthening undergraduate curricula, increasing ACI's academic presence, promoting closer integration between basic immunology and clinical practice, fostering educational innovation, and enhancing collaboration among universities, scientific societies, accreditation bodies, policymakers, and patient organizations. While responsibility for university curricula and specialty recognition remains with national authorities, the EAACI and National Allergy and Immunology Societies, in partnership with patient organizations, can provide scientific leadership, develop educational standards, and advocate for harmonised approaches. The Declaration of Salamanca offers a practical framework to improve the quality, consistency, and sustaina
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Journal articleMassen G, Jenkins G, Stewart I, et al., 2026,
Temporal trends in single and multiple organ fibrosis prevalence and primary care consultations: a population based cohort study of 5·8 million individuals in England
, BMJ Open, ISSN: 2044-6055ObjectiveTo understand how prevalence estimates of single and multiple organ fibrosis have changed from 2012 to 2022.DesignRetrospective population-based cohort studySettingData from primary (Clinical Practice Resource Datalink Aurum) and secondary care (Hospital Episode Statistics Admitted Patient Care) electronic health records were used to conduct this study.ParticipantsAdults age 18 years and over whose primary and secondary care records were available for research.Main outcome measureFibrotic conditions previously determined from a Delphi survey of clinicians; diagnoses were found in either primary or secondary care records. The primary analysis estimated the prevalence of both single and multiple organ fibrosis prevalence. A secondary analysis used Cox proportional hazards models to investigate the association between the time-updated number of fibrotic conditions and risk of death adjusting for age and sex.ResultsThe cohort consisted of 5,839,459 people with at least one fibrotic condition and a denominator of 18,784,962 people. Over the study period prevalence of fibrotic conditions increased by 6.72%, as of 2022, 19·95% (95%CI:19·92 to 19·98) of adults had at least one fibrotic condition. Prevalence of multiple organ fibrosis increased from 4·78% (95%CI:4·76 to 4·79) in 2012 to 8·51% (95%CI:8·50 to 8·53) in 2022. In the year preceding diagnosis of single organ fibrosis, the median number of primary care consultations was 14 compared with 21 consultations for people with multiple organ fibrosis. Compared with people with single organ fibrosis, people with two fibrotic conditions had a mortality hazard ratio of 2.90 (95%CI: 2.87-2.93), whilst people with three fibrotic conditions had a mortality hazard ratio of 5.22 (95% CI:5.14-5.30).ConclusionsPrevalence of single and multiple organ fibrosis has substantially increased over a decade. People with multiple organ fibrosis access healthcare more tha
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Journal articleYie G-E, Kim E, Pham DD, et al., 2026,
Stool and Airway Microbiome Signatures Associated With Treatment Response to Dupilumab in Severe Asthma: Findings From the PRISM Study.
, AllergyBACKGROUND: Severe asthma is characterized by persistent airway inflammation and heterogeneous responses to biologic therapies. Growing evidence implicates the gut-lung axis in asthma pathophysiology; however, few studies have concurrently characterized gut and airway microbiomes in relation to treatment response in severe asthma. METHODS: We profiled microbiomes of stool bacteria (STB), stool-derived extracellular vesicles (STE), and exhaled breath condensate (EBC) from 48 patients with severe asthma receiving dupilumab. Microbial composition, alpha diversity, and predicted functional profiles were compared across sample types and longitudinally according to treatment response. Associations between microbial features and asthma-related clinical markers were also evaluated. RESULTS: Distinct taxonomic and predicted functional signatures were identified across biological compartments. EBC samples were enriched in Proteobacteria, including Pseudomonas, and exhibited a higher predicted abundance of pathways related to two-component systems and bacterial secretion systems. EBC microbial diversity was positively associated with baseline sputum eosinophil levels (p = 0.018), whereas stool microbial richness demonstrated a time-dependent association with blood eosinophil counts after treatment (p for interaction = 0.023). Treatment responders exhibited lower abundances of Lachnospira (STB q = 0.046; STE q = 0.042) and Escherichia-Shigella (STE q = 0.038), and a higher relative abundance of the Oscillospiraceae NK4A214 group (STB q = 5.5 × 10-7, STE q = 1.4 × 10-8) in stool-derived profiles. CONCLUSION: Gut and airway-derived microbiomes appear to play complementary roles in severe asthma. Stool-derived microbial features may reflect systemic inflammatory signals associated with treatment response, whereas airway-derived microbial profile
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Journal articleWu WW, Wang J, Ma WAQ, et al., 2026,
Impact of Cardiovascular Comorbidities on Clinical Outcomes Across the Asthma Spectrum.
, RespirologyBACKGROUND AND OBJECTIVE: Cardiovascular disease (CVD) is a prevalent comorbidity in asthma, yet its impact on clinical outcomes across disease states remains poorly characterised. METHODS: We analysed data from two independent prospective cohorts. Cohort I comprised 1058 stable asthma patients (CVD: n = 107; non-CVD: n = 951) followed for 12 months to assess asthma exacerbations. Cohort II comprised 825 patients hospitalised for an acute exacerbation (CVD: n = 233; non-CVD: n = 592). Missing data were handled by multiple imputation, and the CVD and non-CVD groups were balanced using propensity score overlap weighting. Associations were estimated using negative binomial, gamma, and logistic regression. Mediation and dominance analyses were performed as exploratory analyses. RESULTS: Patients with CVD exhibited greater airflow obstruction and a predominantly non-T2 inflammatory profile characterised by increased neutrophilic inflammation. White blood cells, neutrophils, and monocytes partially mediated the association between CVD and lower FEV1/FVC ratio, while monocytes additionally mediated the association between CVD and severe exacerbations. In Cohort I, CVD was independently associated with severe exacerbations (adjusted IRR = 1.96, 95% CI (1.12, 3.44)), hospitalisations, and emergency visits. In Cohort II, CVD was associated with longer hospital stay (adjusted IRR = 1.14, 95% CI (1.01, 1.30)) and higher direct costs, with stroke and coronary heart disease as leading contributors to prolonged stay. CONCLUSION: CVD is independently associated with worse clinical outcomes across the asthma disease spectrum. These findings support recognition of CVD as an important treatable trait in asthma and highlight the need for integrated cardiopulmonary management.
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Journal articleJosa-Culleré A, Koch S, Demeyer H, et al., 2026,
Interaction of walking activity and long-term air pollution on exacerbation rate in COPD
, ERJ Open Research, Pages: 00813-2026<jats:sec> <jats:title>Background</jats:title> <jats:p>Regular walking activity can improve the prognosis in people with chronic obstructive pulmonary disease (COPD). However, its benefit may be reduced when living in highly polluted areas.</jats:p> </jats:sec> <jats:sec> <jats:title>Aim</jats:title> <jats:p>To assess the combined effects of walking activity and air pollution on the rate of moderate-to-severe exacerbation in COPD.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods</jats:title> <jats:p> This prospective cohort study included 262 people with COPD from five European countries (United Kingdom, Spain, Belgium, Switzerland, Greece). Regular walking activity amount (walking bout step count, walking duration) and intensity (90thpercentile (P90) and average walking speed) was measured at baseline for seven days <jats:italic>via</jats:italic> single wearable devices. Residential concentrations of particulate matter<2.5 µm (PM <jats:sub>2.5</jats:sub> ), black carbon (BC), nitrogen dioxide (NO <jats:sub>2</jats:sub> ) and ozone (O <jats:sub>3</jats:sub> ) were estimated using land-use regression models for the previous two years. Moderate-to-severe exacerbations over a two-year follow-up were obtained from medical records and paper diaries. We estimated the interaction between walking activity and air pollution on long-term exacerbation rate with multivariable mixed-effects negative binomial models. </jats:p>
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Journal articleDunne OM, Fulton CR, Griffin CS, et al., 2026,
Cellular, molecular and functional characteristics of induced pluripotent stem cell derived neurons from refractory chronic cough patients and healthy controls
, ERJ Open Research, Pages: 01356-2026<jats:p>The pathophysiology of refractory chronic cough (RCC) and the aetiology of associated cough hypersensitivity syndrome remains unclear, partly due to the absence of a suitable disease-specific sensory neuronal model. This study was designed to investigate whether induced pluripotent stem cell (iPSC)-derived sensory neurons (iPSC-Ns) from patients with RCC exhibit distinct phenotypic characteristics when compared to those from healthy controls (HC).</jats:p> <jats:p>Peripheral blood samples obtained from patients with RCC and HC were reprogrammed to iPSCs and subsequently differentiated into sensory neurons using defined culture conditions over 40 days. The neurogenic differentiation and functional characteristics of the iPSC-Ns were confirmed using molecular assays, live cell calcium mobilisation assays and patch clamp recordings. Transcriptomic differences between RCC and HC derived iPSC-Ns were assessed by RNA-sequencing.</jats:p> <jats:p>Successful differentiation of iPSC-Ns from iPSCs was observed as cells acquired a neuronal morphology, neuronal gene expression (peripherin), the neuronal marker β3-tubulin, and functional sodium channels. TRPV1 and P2X3 responses were heightened in RCC derived iPSC-Ns compared to HC with responses to capsaicin or αβmeATP blocked by the antagonists capsazepine or AF-353 respectively. Differential expression of 853 genes was noted between RCC- and HC-derived iPSC-Ns, with genes enriched in RCC-derived iPSC-Ns associated with sensory neuronal functions.</jats:p> <jats:p>Generation of an iPSC derived neuronal model from patients with RCC is feasible and offers insights into the pathophysiology of cough hypersensitivity syndrome. Heightened purinergic responses observed in iPSC-Ns from RCC compared to HC are consistent with the concept of cough hypersensitivity and support targeting P2X3 receptors as a therapeutic strat
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Journal articleDean C, Chen Q, Tseng P, et al., 2026,
Lung derived extracellular vesicles have distinct pro-repair effects, depending on the age of their source tissue
, npj Regenerative Medicine, ISSN: 2057-3995
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