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Journal articleSuh M, Oh J-Y, Won H-K, et al., 2026,
Patient-Anchored Cough Visual Analogue Scale and Leicester Cough Questionnaire Thresholds for Cough Control Classification in Chronic Cough.
, Lung, Vol: 204PURPOSE: The cough severity visual analogue scale (VAS) and the Leicester Cough Questionnaire (LCQ) are commonly used in chronic cough. While continuous scores are useful for tracking change, categorization is needed to define clinically relevant states. However, patient-anchored thresholds for cough control remain undefined. METHODS: Using the Korean Chronic Cough Registry (n = 890), we derived VAS and LCQ cutoffs anchored to a patient-reported cough control item. Receiver operating characteristic (ROC) analyses were performed using operational definitions of very well-controlled cough ("strongly agree" vs. all others), well-controlled cough ("strongly agree" + "agree" vs. all others), and uncontrolled cough ("disagree" + "strongly disagree" vs. all others). RESULTS: Both scores demonstrated stepwise gradients across cough control categories (p < 0.001). ROC-derived cutoffs for very well-controlled cough were VAS ≤ 10 (area under the curve [AUC], 0.911) and LCQ ≥ 15.8 (AUC, 0.877). For well-controlled cough, the corresponding cutoffs were VAS ≤ 30 (AUC, 0.866) and LCQ ≥ 15 (AUC, 0.856). For uncontrolled cough, the cutoffs were VAS ≥ 50 (AUC, 0.879) and LCQ ≤ 13.0 (AUC, 0.872). Cutoffs were consistent across newly referred chronic cough and refractory chronic cough subgroups. Concordance between VAS- and LCQ-derived classifications was moderate-to-substantial (weighted kappa = 0.55). CONCLUSION: Based on these findings, we propose a patient-anchored classification framework for cough control: very well-controlled cough (VAS ≤ 10, LCQ ≥ 16), well-controlled cough (VAS 11-30, LCQ 15.0-15.9), intermediate cough control (VAS 31-49, LCQ 13.1-14.9), and uncontrolled cough (VAS ≥ 50, LCQ ≤&th
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Journal articleBloom CI, Foer D, Aroda VR, et al., 2026,
It's more than mechanics: the case for metabolic endpoints in airways disease
, European Respiratory Journal, ISSN: 0903-1936 -
Journal articleEvison M, Naylor R, Malcolm R, et al., 2026,
Health economic model to evaluate the cost-effectiveness of smoking cessation services integrated within lung cancer screening in the United Kingdom.
, Thorax, Vol: 81, Pages: 758-765INTRODUCTION: Integrating smoking cessation supports into lung cancer screening can improve abstinence rates. However, healthcare decision-makers need evidence of cost-effectiveness to understand the cost/benefit of adopting this approach. METHODS: To evaluate the cost-effectiveness of smoking cessation interventions, and service delivery, we used a cohort-based Markov model, adapted from previous National Institute for Health and Care Excellence (NICE) guidelines on smoking cessation. This uses long-term epidemiological data to capture the prevalence of the smoking-related illnesses, updated through targeted literature searches as required from the core NICE model, with costs extracted from publicly recognised UK sources. RESULTS: All smoking cessation interventions appeared cost-effective at a threshold of £20 000 per quality-adjusted life year, compared with no intervention or behavioural support alone. Offering immediate smoking cessation as part of lung cancer screening appointments, compared with usual care (onward referral to stop smoking services), was also estimated to be cost-effective with a net monetary benefit of £2198 per person, and a saving of between £34 and £79 per person in reduced workplace absenteeism among working age attendees. Estimated healthcare cost savings were more than four times greater in the most deprived quintile compared with the least deprived, alongside a fivefold increase in quality adjusted life years accrued. CONCLUSIONS: Smoking cessation interventions within lung cancer screening are cost-effective and should be integrated, so that treatment is initiated during screening visits. This is likely to reduce overall costs to the health service, and wider integrated care systems, improve quality and length of life, and may lessen health inequalities.
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Journal articleDribin TE, Sobolewski B, Campbell RL, et al., 2026,
Anaphylaxis Clinical Care Pathway: Incorporating Intranasal Epinephrine (Adrenaline).
, J Allergy Clin Immunol PractHealth care providers across settings must be trained to manage anaphylaxis by (1) removing the offending allergen if still present; (2) positioning the patient with legs elevated, and if respiratory distress is present, allow the patient to sit upright with legs extended and elevated; (3) immediately administering epinephrine (adrenaline) intramuscularly (IM) or intranasally (IN) every 5 to 15 minutes for persistent anaphylaxis; and (4) optimizing airway, breathing, and cardiovascular (ABC) resuscitation. This may include supplemental oxygen, noninvasive or invasive positive-pressure ventilation, and intravenous fluid resuscitation. For life-threatening or refractory presentations, (5) IM/IN epinephrine should be administered every 5 minutes while addressing ABC derangements; this includes aggressive intravenous fluid resuscitation for patients in anaphylactic shock. Providers may continue IM or IN epinephrine or switch to the other, as both routes are considered equally efficacious based on pharmacokinetic data. An intravenous epinephrine infusion should be prepared for patients with persistent anaphylaxis after 2 doses of IM/IN epinephrine and initiated after the third dose, or earlier at the provider's discretion. In settings without epinephrine infusions, repeat IM/IN epinephrine should be administered every 5 minutes, along with other ABC interventions, and the patient should be transferred quickly to a setting equipped to provide advanced resuscitative care.
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Journal articleLau R, Giblin S, Sugar A, et al., 2026,
SpyCEP dismantles neutrophil immunity via disorder-driven chemokine remodeling and GAG targeting
, Proceedings of the National Academy of Sciences of the United States of America, Vol: 123, ISSN: 0027-8424Streptococcus pyogenes evades neutrophil-mediated immunity by secreting the protease SpyCEP, which inactivates chemokines such as CXCL8; however, the mechanism by which SpyCEP targets CXCL8 for cleavage has remained unclear. This work uncovers an intrinsically disordered autocatalytic maturation loop that binds CXCL8 and induces a conformationally heterogeneous state in the chemokine. A model is proposed in which this disorder-mediated recognition facilitates access to the substrate cleavage site and is compatible with SpyCEP acting at glycosaminoglycan (GAG)-bound CXCL8 reservoirs. This disorder-mediated mode of substrate recognition departs from classical protease–substrate interfaces and identifies the SpyCEP cleaved autocatalytic matu-ration loop (CAML) as a potential target for anti-virulence strategies against S. pyogenes.
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Journal articleAdegunsoye A, Oldham JM, Aracena KA, et al., 2026,
Longitudinal Mediastinal Lymph Node Dynamics Associate With Mortality and Fibrosis Progression in Fibrotic Interstitial Lung Disease.
, ChestBACKGROUND: Although mediastinal lymph node (MLN) enlargement is common in fibrotic interstitial lung disease (ILD), its dynamic behavior and prognostic value are unclear. RESEARCH QUESTION: Do MLN size, count, and progression on high-resolution chest CT imaging associate with physiological decline, fibrosis progression, and transplant-free survival, and do these factors improve risk models? STUDY DESIGN AND METHODS: This study included a prospective cohort of patients with fibrotic ILD from a tertiary center (N = 1,122) with independent replication (n = 181). MLNs were scored by using standardized radiologic criteria; fibrosis was quantified according to deep texture analysis. Associations with outcomes were evaluated by using Cox and linear mixed-effects models; model discrimination was assessed by using Harrell's concordance index and net benefit by decision curve analysis. RESULTS: Baseline MLN enlargement (≥ 10 mm) occurred in 67% and was independently associated with worse transplant-free survival (hazard ratio, 2.44; 95% CI, 2.01-2.96; P < .0001). MLN progression was associated with excess mortality (adjusted hazard ratio, 4.09; 95% CI, 2.34-7.17; P < .001) and modified the association between fibrosis progression and survival (interaction hazard ratio, 3.02; P = .001). Fibrosis remained the stronger prognostic marker, but MLN metrics added complementary information within fibrosis strata and modestly improved discrimination when added to clinical models based on ILD-GAP (gender, age, physiology) model score or progressive pulmonary fibrosis status. Findings were directionally consistent in the independent replication cohort. INTERPRETATION: MLN burden and progression are accessible, quantifiable imaging biomarkers associated with adverse outcomes in fibrotic ILD. Incorporating MLN metrics into existing clinical models improves risk discrimination and supports further evaluation of their role in ILD risk stratification.
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Journal articleMathur V, Molyneaux PL, Cassella J, 2026,
Nalbuphine for Cough Caused by Idiopathic Pulmonary Fibrosis-Reply.
, JAMA, Vol: 336 -
Journal articleGuerrero-Fonseca IM, Hernández-Almaraz KB, León-Vega II, et al., 2026,
Neutrophil serine proteases degrade endothelial cortactin and promote extravasation.
, J Cell Biol, Vol: 225The adhesive interactions of neutrophils with postcapillary venules during inflammation have been well studied. However, how neutrophils trigger molecular changes in endothelial cells (EC) during their extravasation requires further exploration. The endothelial actin-binding protein cortactin regulates endothelial contacts and neutrophil-endothelial interactions, but the associated mechanisms remain elusive. Hypothesizing that endothelial cortactin dynamics change during inflammation, using super-resolution confocal microscopy of inflamed mouse cremasteric venules and HUVEC, we report that neutrophil interaction with EC induces reduction in EC cortactin levels. This response was specifically mediated by neutrophil serine proteases, including cathepsin G, that were detected inside EC. The observed cortactin degradation was abolished after inhibition of serine proteases or blockade of neutrophil exocytosis. Finally, the endogenous serine protease inhibitor α1-antitrypsin suppressed cortactin degradation in vivo and reduced neutrophil adhesion and extravasation. Collectively, our data unveil a new mechanism by which neutrophils manipulate proteins inside EC to facilitate their extravasation.
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Journal articleWells C, Rosewarne C, Taylor K, et al., 2026,
Swimming against the tide in implementing change in paediatric physiotherapy for asthma and dysfunctional breathing: stakeholder reflections through digital storytelling
, Design for Health, Pages: 1-13, ISSN: 2473-5132 -
Journal articleCheong S-S, Yan C, Mongey R, et al., 2026,
TGF-alpha/EGFR signalling mediates retinoic acid-induced lung repair
, npj Regenerative Medicine, ISSN: 2057-3995Lung repair involves coordination of multicellular processes, including endothelial angiogenesis and epithelial repopulation. Retinoic acid (RA) signalling is crucial for lung development, homeostasis, and repair, however, the mechanisms through which RA drives repair are still unknown. It has previously been shown that RA has no direct effects on repair of alveolar epithelium, yet in animal studies, RA induces alveolar regeneration. Here we show that RA induces endothelial angiogenesis, which is associated with enhanced paracrine signalling to alveolar epithelial cells. Transcriptomic profiling of RA-treated HPMECs undergoing angiogenesis revealed enrichment of wound healing pathways and subsequent in-silico analysis identified several candidate mediators of endothelial-epithelium crosstalk. Scratch assays demonstrated that of these candidates, only TGFα promoted wound healing in alveolar epithelial A549 and primary human alveolar type 2 (hAT2) cells. Mechanistically, TGFα was associated with increased epithelial cell migration and activation of EGFR signalling, without detectable effects on proliferation or apoptosis. Our findings indicate that RA-induced endothelial angiogenesis promotes epithelial EGFR signalling through paracrine mediators, including TGFα. This study highlights the importance of endothelial–epithelial interactions in lung repair and provides insight into pathways that may be targeted to enhance alveolar regeneration.
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Journal articleLeung AS-Y, Tham EH, Yamamoto-Hanada K, et al., 2026,
Global Variation in Timing of Allergenic Food Introduction for Food Allergy Prevention: An International Survey of Healthcare Professionals.
, AllergyBACKGROUND: IgE-mediated food allergy prevention guidelines are now established in many countries, but their implementation in routine clinical practice globally remains unclear. METHODS: An anonymous online survey was distributed to healthcare professionals (HCPs) through the World Allergy Organization network between December 2024 and April 2025, collecting data on food allergy prevention recommendations in daily clinical practice. RESULTS: The analysis included 731 healthcare professionals from 80 countries worldwide: Asia (36.7%), Europe (27.1%), North America (15.9%), and Rest of the World (20.0%; Russia, South America, Africa, Oceania). Unsupervised clustering revealed two distinct practice patterns-one favoring early allergen introduction and one favoring later introduction-with timing varying by allergen type. For peanuts, clusters diverged between early (median 6 months of age) and late (median 18 months of age) introduction recommendations for high-risk infants. Allergen introduction timing was independently driven by region and specialty: North American HCPs recommend peanut introduction 6.7 months earlier than those in Asia (5.48 ± $$ \pm $$ 3.32 vs. 12.18 ± $$ \pm $$ 7.27 months; p < 0.001), and pediatric allergists globally advocate for introduction 2.37 months earlier than non-allergists (8.72 ± $$ \pm $$ 5.85 vs. 11.09 ± $$ \pm $$ 7.14 months, p = 0.024). This disparity is more pronounced in high-risk infants than in normal-risk infants. CONCLUSIONS: The variability in allergen introduction practices, driven by geography and medical specialty, highlights a persistent gap in prevention guidelines adoption. This divergence likely reflects both suboptimal implementation of existing recommendations and regional differences in food allergy epidemiology. These findings underscore the need for population-tailored allergen introduction strategies acro
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Journal articleWawman RE, Shah PL, Boffito M, et al., 2026,
The relationship between plasma favipiravir concentrations and clinical outcomes in COVID-19
, ERJ Open Research, Vol: 12, ISSN: 2312-0541BackgroundFavipiravir has shown efficacy against SARS-CoV-2 in patients <60 years old, but data linking plasma concentrations to clinical outcomes are limited. This study investigated whether favipiravir plasma concentrations influence clinical efficacy and outcomes in patients hospitalised with COVID-19. The main research question was, How can antiviral dosing strategies be optimised to improve pandemic preparedness and treatment efficacy?MethodsAdult participants were drawn from the PIONEER trial, in which patients received oral favipiravir (1800 mg twice daily for 1 day, then 800 mg twice daily for 9 days) plus standard care. This analysis included patients with confirmed COVID-19 and ≥75% study adherence. Samples were collected between days 5 and 10 post-treatment initiation. The primary outcome was time to clinical improvement. Secondary outcomes included achievement of clinical improvement and mortality risk.ResultsOut of 140 patients (50% male; mean±sd age 59.5±14.8 years), target plasma concentrations were reached in 29 (21%). Mean time to improvement was 7.7±5.9 days in target achievers versus 9.1±7.2 days in non-achievers (p=0.26). The target was more often achieved in female (34%) than male (7%) participants (p=0.0002). Plasma concentration inversely correlated with body mass index (r= –0.4, p<0.0001), and with lower body mass index in achievers (26.0±5.1 kg·m−2 versus 30.5±6.9 kg·m−2, p=0.003). Alkaline phosphatase and alanine aminotransferase levels were also lower in achievers (p=0.004 and p=0.02, respectively).ConclusionMost patients did not reach target favipiravir levels. Concentrations were influenced by sex, body mass index and liver function, confirming the need for pharmacokinetically guided dosing and therapeutic monitoring to optimise antiviral efficacy in future pandemic responses.
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Journal articleWang M, Hu H, Wang K, et al., 2026,
Deficiency of Mitochondrial Fatty Acid Enzyme, CPT1A, Underlies Airway Epithelial Barrier Dysfunction in Severe Asthma.
, AllergyBACKGROUND: Mitochondrial fatty acid oxidation through carnitine palmitoyltransferase-1A (CPT1A) leads to ATP generation. We examined its role in regulating permeability and mitochondrial metabolic homeostasis of airway epithelial cells in asthma. METHODS: Primary nasal epithelial cells (NECs) from healthy controls and severe asthma (SA) patients in air-liquid interface (ALI) were exposed to CPT1A siRNA/CPT1A overexpression lentiviral/L-carnitine (LCA). Epithelial TEER and FITC-dextran transport were measured. Bronchial biopsies from healthy and SA subjects and house dust mite (HDM) asthma mouse model were also studied. RESULTS: In NECs-ALI and in bronchial epithelial cells (BECs) from bronchial biopsies of SA, CPT1A expression was reduced compared to healthy controls. Knock-down of CPT1A in healthy NECs reduced expression of Occludin and E-cadherin and impaired epithelial barrier integrity (EBI), while upregulation of CPT1A with CPT1A overexpression lentiviral/LCA in SA-NECs increased the barrier proteins with improved EBI. CPT1A knockdown in healthy BECs increased release of mtROS, with mitochondrial disruption and activation of ERK1/2-NF-κB signaling pathway. These were aggravated with HDM exposure but N-acetyl-cysteine and MitoTempo reduced p-ERK1/2 and p-P65 activation, as well as EBI with CPT1A knockdown and HDM. In the mouse model, there was decreased airway epithelial CPT1A protein expression, associated with reduced airway hyperreactivity and inflammation, and in Occludin and ZO-1 expression, effects partly reversed by LCA, with restoration of mitochondrial integrity and EBI. CONCLUSION: CPT1A maintains epithelial barrier function through restoration of mitochondrial function in asthmatic airway epithelial cells. Restoration of deficient epithelial CPT1A of SA may represent a new treatment approach.
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Journal articleTanskanen E, Sun H, Cheng K-C, et al., 2026,
Co-formulation of IL-12 mRNA and doxorubicin in polymeric nanoparticles for simultaneous delivery in murine melanoma
, RSC Pharmaceutics, ISSN: 2976-8713Liposomal or polymeric nanoparticles have been instrumental in improving delivery of poorly soluble chemotherapeutics and those with dose limiting toxicity such as doxorubicin (DOX). More recently, nanoformulations have shown to enable simultaneous delivery of emerging biomolecules such as siRNA. However, for larger nucleic acids such as mRNA this remains challenging. In this study, we developed a poly(β-amino ester) (PBAE) based platform, capable of co-formulation of mRNA and doxorubicin into nanoparticles. To demonstrate proof of concept using therapeutically relevant cargo, immunomodulatory interleukin-12 (IL-12) was selected as a model mRNA. IL-12 is a pro-inflammatory cytokine that promotes anti-tumour immunity partly through amplifying effector cytokines such as interferon-γ (IFNγ). We found that PBAE complexed DOX and mRNA into positively charged nanoparticles of 120 nm and size-exclusion chromatography indicated a DOX loading efficiency of over 97%. Co-association of both DOX and mRNA was characterised at a single nanoparticle level by nano-flow cytometry. Following delivery to B16F10 murine melanoma cells, more than 95% of cells were double positive for DOX and cy5-labelled mRNA, and confocal microscopy confirmed co-localised regions of DOX with mRNA. Interestingly, nanoformulated DOX had increased nuclear accumulation by 1.7-fold relative to free DOX which correlated with a significantly reduced cell viability of 12.9% with PBAE-DOX/mRNA, compared to 26.6% for free DOX at the same dose. Moreover, despite this strong cytotoxic effect, reporter mRNA translation remained robust, with luciferase expression approximately two orders of magnitude above non-transfected controls at the highest DOX doses. Co-formulation of IL-12 mRNA and DOX with PBAE demonstrated effective IL-12 protein secretion in transfected B16F10 cells with simultaneous DOX dose dependent reduction in viability. Secreted IL-12 was bioactive, inducing dose dependent STAT4 pho
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Journal articleCarlsten C, Salvi S, Wong GWK, et al., 2026,
Supplements and medications for respiratory resilience against air pollution.
, ERJ Open Res, Vol: 12, ISSN: 2312-0541Air pollution is a major threat to respiratory health. In this article, we review the current literature on accessible interventions that could help patients build resilience against this threat. We explore the potential benefits of antioxidant-rich diets, including supplements such as fish oil, vitamins C, D and E, and prebiotics, which have shown promise in reducing inflammation and oxidative stress, thereby mitigating air pollution-related respiratory decline. Nasal washes are commonly used to clear nasal passages, which could help to clear pollutants from the nasal passages and improve mucociliary clearance. Furthermore, medications such as nonsteroidal anti-inflammatory drugs and intranasal corticosteroids have been reported to reduce pollutant-related airway inflammation and lung function deterioration triggered by pollutant exposure. Given the generally favourable safety profile of these interventions, they are reasonable to consider in consultation with a care provider. Further research is needed to establish optimal dosing, safety and long-term efficacy, particularly for those exposed to chronic air pollution. Healthcare professionals should work together to further identify and implement effective interventions to mitigate the impact of air pollution on respiratory health.
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Journal articleGardiner LE, Lozano-Rojas D, Smith N, et al., 2026,
Investigating prognostic classifications of preexisting multiple long-term conditions for health outcomes 1 year after COVID-19 hospitalization: A UK prospective observational study.
, Int J Infect Dis, Vol: 168BACKGROUND: Preexisting multiple (two or more) long-term conditions (MLTCs) may negatively affect recovery after COVID-19. We investigated how preexisting MLTCs, including different categorization and patterns of MLTCs, affect 1-year health outcomes after severe COVID-19. METHODS: Adults post-hospitalization after COVID-19 were recruited during 2020-2021. We compared recovery at 1 year after discharge using adjusted multivariable logistic regression in 1:1 propensity-matched adults (for age, sex, ethnicity, social deprivation, obesity, and smoking history) with and without preexisting MLTCs. In adults with MLTCs, different categorization such as number of conditions, number and types of body systems involved (e.g. respiratory, cardiovascular), and latent class analysis-derived patterns of condition co-occurrence were assessed for their association with recovery at 1 year. RESULTS: A total of 647 adults with MLTCs were matched with 647 adults without MLTCs (n = 1294; 61.9% male, 79.6% of White ethnicity, median age 59 [interquartile range 52-67] years). The presence of MLTCs was associated with lower odds of feeling fully recovered (odds ratio 0.66 [95% confidence interval 0.51-0.85], P = 0.001). In those with MLTCs, recovery was negatively affected by number and type of body systems involved (e.g. respiratory [odds ratio 0.49 (95% confidence interval 0.34-0.69), P <0.001]) but not by the number of conditions (P >0.1). Four latent classes of MLTC co-occurrence were estimated with different risks of recovery (P <0.01). CONCLUSION: Adults with preexisting MLTCs were 34% less likely to feel fully recovered at 1 year after COVID-19 hospitalization than adults without MLTCs. We describe prognostic classifications of MLTCs, with future work needed to understand whether they have prognostication in broader post-acute infection sequalae.
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Journal articleKlimek L, Mullol J, Reitsma S, et al., 2026,
Correspondence: The First Biosimilar for Biologics in Allergy: CT-P39 (Omlyclo-Omalizumab-Igec) Is Available for Asthma, Chronic Spontaneous Urticaria, and Chronic Rhinosinusitis With Nasal Polyps.
, Allergy, Vol: 81, Pages: 2568-2570 -
Journal articlede Benedictis FM, Beasley R, Pavord I, et al., 2026,
50 years on: how inhaled corticosteroids have changed the treatment of asthma.
, Lancet Respir Med, Vol: 14, Pages: 633-646Inhaled corticosteroids are the foundation of asthma therapy and now, 50 years on from their introduction, is an appropriate time to summarise some of the key studies that have progressed the field. We can now make better decisions in selecting the optimal inhaled corticosteroid-based regimens and identifying likely responders, based on biomarkers and patient characteristics. Inhaled corticosteroids reduce the risk of asthma attacks, but do not alter the course of the disease. Asthma remission, which is as yet an undefined therapeutic goal, is the aim, but the role of inhaled corticosteroids is unclear. High-dose inhaled corticosteroid therapy can cause systemic adverse events, suggesting that steps be taken to avoid this through the addition of long-acting β2-adrenergic agonists and the judicious use of biologics. Researchers will continue to learn more about the advantages and limitations of inhaled corticosteroids as they explore methods of disease prevention and remission in the future with new tools and treatments.
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Journal articleYang W, Giblin SP, Pease JE, 2026,
Evidence for a Two-Step Model for Activation of GPR25 by the Chemoattractant CXCL17.
, Basic Clin Pharmacol Toxicol, Vol: 139CXCL17 was recently reported to activate GPR25, a receptor expressed by T-regulatory cells. Although classified as a chemokine, the activity of CXCL17 is ablated by minor C-terminal truncation, suggesting a novel mode of receptor activation. We set out to test this hypothesis by mutagenesis. GPR25 was expressed in the murine pre-B cell line L1.2 and mediated robust migration of transfectants to nanomolar concentrations of recombinant CXCL17 (24-119). The N-terminally truncated form of CXCL17 (64-119) was also chemotactic for GPR25 transfectants, albeit with severely reduced potency. Modelling of CXCL17:GPR25 implied multiple interactions between the N- and C-termini of CXCL17 with GPR25, which was validated by mutagenesis. Cells expressing a chimeric FPR1:GPR25 construct responded chemotactically to CXCL17 but with significantly reduced potency compared with wild-type GPR25 transfectants, implicating the GPR25 N-terminus in CXCL17 recognition. Mutagensis of the GPR25 residues W95, R178 and R264 resulted in a complete loss of chemotactic responsiveness to CXCL17, consistent with the residues interacting with the C-terminal CXCL17 motif. In conclusion, we verify GPR25 as a bona fide CXCL17 receptor and suggest a two-step model of GPR25 activation, in which the receptor N-terminus orients CXCL17 for activation of GPR25 via its C-terminus. We also advocate the reclassification of CXCL17 as a chemoattractant distinct from the chemokine family.
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Journal articleChung KF, 2026,
From the London International Cough Symposium to the ERS Cough Conference: chronic cough comes of age.
, ERJ Open Res, Vol: 12, ISSN: 2312-0541The @EuroRespSoc Cough Conference https://bit.ly/4asS7NF.
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