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Conference paperPyle CJ, Patel ND, Edwards MR, et al., 2024,
A Rhinovirus VP0 Vaccine Induces Cross-reactive Type 1 Immunity and Promotes Lymphocyte Activation and Maturation
, International Conference of the American-Thoracic-Society (ATS), Publisher: AMER THORACIC SOC, ISSN: 1073-449X -
Conference paperChoy D, Nazarova E, Grimbaldeston M, et al., 2024,
A Stop-gain in FUT2 Associates With Several COPD Related Phenotypes and Clinical Outcomes
, International Conference of the American-Thoracic-Society (ATS), Publisher: AMER THORACIC SOC, ISSN: 1073-449X -
Conference paperMar J, Dugger D, Chen H, et al., 2024,
Longitudinal Effects of Experimental Rhinovirus Challenge on Airway Phenotype in Chronic Obstructive Pulmonary Disease
, International Conference of the American-Thoracic-Society (ATS), Publisher: AMER THORACIC SOC, ISSN: 1073-449X -
Conference paperBell J, Graul E, Nordon C, et al., 2024,
EXACOS CARBON: Describing the Greenhouse Gas Emissions of Healthcare Resource Utilization by Frequency and Severity of COPD Exacerbation in England
, International Conference of the American-Thoracic-Society (ATS), Publisher: AMER THORACIC SOC, ISSN: 1073-449X -
Journal articleCass SP, Nicolau DV, Baker JR, et al., 2024,
Coordinated nasal mucosa-mediated immunity accelerates recovery from COVID-19
, ERJ OPEN RESEARCH, Vol: 10 -
Conference paperThillai M, Oldham J, Ruggiero A, et al., 2024,
Deep Learning-based Segmentation of CT Scans Predicts Disease Progression and Mortality in IPF
, International Conference of the American-Thoracic-Society (ATS), Publisher: AMER THORACIC SOC, ISSN: 1073-449X -
Conference paperMacKay J, Jucaite A, Cselenyi Z, et al., 2024,
FIRST-TIME-IN-HUMAN VISUALISATION OF CCR9 EXPRESSION IN THE GUT BY POSITRON EMISSION TOMOGRAPHY
, Digestive Disease Week (DDW), Publisher: W B SAUNDERS CO-ELSEVIER INC, Pages: S605-S605, ISSN: 0016-5085 -
Journal articleJia M, Fu H, Jiang X, et al., 2024,
DEL-1, as an anti-neutrophil transepithelial migration molecule, inhibits airway neutrophilic inflammation in asthma
, Allergy, Vol: 79, Pages: 1180-1194, ISSN: 0105-4538BackgroundNeutrophil migration into the airways is a key process in neutrophilic asthma. Developmental endothelial locus-1 (DEL-1), an extracellular matrix protein, is a neutrophil adhesion inhibitor that attenuates neutrophilic inflammation.MethodsLevels of DEL-1 were measured in exhaled breath condensate (EBC) and serum in asthma patients by ELISA. DEL-1 modulation of neutrophil adhesion and transepithelial migration was examined in a co-culture model in vitro. The effects of DEL-1-adenoviral vector-mediated overexpression on ovalbumin/lipopolysaccharide (OVA/LPS)-induced neutrophilic asthma were studied in mice in vivo.ResultsDEL-1 was primarily expressed in human bronchial epithelial cells and was decreased in asthma patients. Serum DEL-1 concentrations were reduced in patients with severe asthma compared with normal subjects (567.1 ± 75.3 vs. 276.8 ± 29.36 pg/mL, p < .001) and were negatively correlated to blood neutrophils (r = −0.2881, p = .0384) and neutrophil-to-lymphocyte ratio (NLR) (r = −0.5469, p < .0001). DEL-1 concentrations in the EBC of severe asthmatic patients (113.2 ± 8.09 pg/mL) were also lower than normal subjects (193.0 ± 7.61 pg/mL, p < .001) and were positively correlated with the asthma control test (ACT) score (r = 0.3678, p = .0035) and negatively related to EBC IL-17 (r = −0.3756, p = .0131), myeloperoxidase (MPO) (r = −0.5967, p = .0055), and neutrophil elastase (NE) (r = −0.5488, p = .0009) expression in asthma patients. Neutrophil adhesion and transepithelial migration in asthma patients were associated with LFA-1 binding to ICAM-1 and inhibited by DEL-1. DEL-1 mRNA and protein expression in human bro
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Journal articleManeechotesuwan K, Prapruetkit N, Chankham J, et al., 2024,
Paradoxical eosinophilic and cytokine responses to oral corticosteroid treatment in patients with asthma exacerbations
, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY: GLOBAL, Vol: 3- Cite
- Citations: 2
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Journal articleKing GG, Chung LP, Usmani OS, et al., 2024,
Improving asthma outcomes: Clinicians' perspectives on peripheral airways
, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY: GLOBAL, Vol: 3- Cite
- Citations: 5
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Journal articleRoth-Walter F, Adcock IM, Benito-Villalvilla C, et al., 2024,
Metabolic pathways in immune senescence and inflammaging: novel therapeutic strategy for chronic inflammatory lung diseases. An EAACI position paper from the Task Force for Immunopharmacology
, Allergy, Vol: 79, Pages: 1089-1122, ISSN: 0105-4538The accumulation of senescent cells drives inflammaging and increases morbidity of chronic inflammatory lung diseases. Immune responses are built upon dynamic changes in cell metabolism that supply energy and substrates for cell proliferation, differentiation, and activation. Metabolic changes imposed by environmental stress and inflammation on immune cells and tissue microenvironment are thus chiefly involved in the pathophysiology of allergic and other immune-driven diseases. Altered cell metabolism is also a hallmark of cell senescence, a condition characterized by loss of proliferative activity in cells that remain metabolically active. Accelerated senescence can be triggered by acute or chronic stress and inflammatory responses. In contrast, replicative senescence occurs as part of the physiological aging process and has protective roles in cancer surveillance and wound healing. Importantly, cell senescence can also change or hamper response to diverse therapeutic treatments. Understanding the metabolic pathways of senescence in immune and structural cells is therefore critical to detect, prevent, or revert detrimental aspects of senescence-related immunopathology, by developing specific diagnostics and targeted therapies. In this paper, we review the main changes and metabolic alterations occurring in senescent immune cells (macrophages, B cells, T cells). Subsequently, we present the metabolic footprints described in translational studies in patients with chronic asthma and chronic obstructive pulmonary disease (COPD), and review the ongoing preclinical studies and clinical trials of therapeutic approaches aiming at targeting metabolic pathways to antagonize pathological senescence. Because this is a recently emerging field in allergy and clinical immunology, a better understanding of the metabolic profile of the complex landscape of cell senescence is needed. The progress achieved so far is already providing opportunities for new therapies, as well as for st
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Journal articleSuh DI, Johnston SL, 2024,
The Wiser Strategy of Using Beta-Agonists in Asthma: Mechanisms and Rationales
, ALLERGY ASTHMA & IMMUNOLOGY RESEARCH, Vol: 16, Pages: 217-234, ISSN: 2092-7355 -
Conference paperHarper AR, Bouma G, Lundahl A, et al., 2024,
TOLERABILITY, SAFETY, AND CLINICAL PHARMACOLOGY OF AZD7798, A DEPLETING ANTIBODY TARGETING CCR9
, Digestive Disease Week (DDW), Publisher: W B SAUNDERS CO-ELSEVIER INC, Pages: S816-S817, ISSN: 0016-5085 -
Journal articlePinkerton JW, Preite S, Piras A, et al., 2024,
PI3Kγδ inhibition suppresses key disease features in a rat model of asthma
, Respiratory Research, Vol: 25, ISSN: 1465-9921BACKGROUND: Two isoforms of Phosphoinositide 3-kinase (PI3K), p110γ and p110δ, are predominantly expressed in leukocytes and represent attractive therapeutic targets for the treatment of allergic asthma. The study aim was to assess the impact of administration of an inhaled PI3Kγδ inhibitor (AZD8154) in a rat model of asthma. METHODS: Firstly, we checked that the tool compound, AZD8154, inhibited rat PI3K γ & δ kinases using rat cell-based assays. Subsequently, a time-course study was conducted in a rat model of asthma to assess PI3K activity in the lung and how it is temporally associated with other key transcription pathways and asthma like features of the model. Finally, the impact on lung dosed AZD8154 on target engagement, pathway specificity, airway inflammation and lung function changes was assessed. RESULTS: Data showed that AZD8154 could inhibit rat PI3K γ & δ isoforms and, in a rat model of allergic asthma the PI3K pathway was activated in the lung. Intratracheal administration of AZD8154 caused a dose related suppression PI3K pathway activation (reduction in pAkt) and unlike after budesonide treatment, STAT and NF-κB pathways were not affected by AZD8154. The suppression of the PI3K pathway led to a marked inhibition of airway inflammation and reduction in changes in lung function. CONCLUSION: These data show that a dual PI3Kγδ inhibitor suppress key features of disease in a rat model of asthma to a similar degree as budesonide and indicate that dual PI3Kγδ inhibition may be an effective treatment for people suffering from allergic asthma.
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Journal articleDelfini Cancado JE, Usmani OS, 2024,
Choice of inhaler device and its disposal have a significant impact on the environment
, JORNAL BRASILEIRO DE PNEUMOLOGIA, Vol: 50, ISSN: 1806-3713 -
Journal articleWilliams P, Buttery SC, Hopkinson N, et al., 2024,
Lung disease and social justice - COPD as a manifestation of structural violence
, American Journal of Respiratory and Critical Care Medicine, Vol: 209, Pages: 938-946, ISSN: 1073-449XLung health, the development of lung disease, and how well a person with lung disease is able to live, all depend on a wide range of societal factors. These systemic factors that adversely affect people and cause injustice, can be thought of as “structural violence”. To make the causal processes relating to COPD more apparent, and the responsibility to interrupt or alleviate them clearer, we have developed a taxonomy to describe this. It contains five domains: 1)Avoidable lung harms: (i)processes impacting on lung development (ii)processes which disadvantage lung health in particular groups across the life course. 2)Diagnostic Delay: (i)healthcare factors (ii)norms and attitudes that mean that COPD is not diagnosed in a timely way, denying people with COPD effective treatment. 3)Inadequate COPD Care: ways in which the provision of care for people with COPD falls short of what is needed to ensure that they are able to enjoy the best possible health, considered as (i)healthcare resource allocation (ii)norms and attitudes influencing clinical practice. 4)Low status of COPD: ways both COPD as a condition and people with COPD are held in less regard and considered less of a priority than other comparable health problems. 5)Lack of Support: factors that make living with COPD more difficult than it should be (i)socioenvironmental factors (ii)factors that promote social isolation. This model has relevance for policymakers, healthcare professionals and the public as an educational resource, to change clinical practices and priorities and to stimulate advocacy and activism with the goal of the elimination of COPD.
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Journal articleWilliams P, Bachir L, Cumella A, et al., 2024,
Impact of omitting annual reviews for COPD on patient reported care quality – outcomes from the Asthma+Lung COPD patient passport
, BMJ Open, Vol: 14, ISSN: 2044-6055Background: Regular clinical reviews of people with COPD provide an opportunity to optimise management and are recommended in national and international guidelines. However, there are limited data about the relationship between having an annual review and other aspects of care quality, which might influence decision making by healthcare professionals and commissioners.Method: Using data from 74,827 people with COPD completing the Asthma + Lung UK COPD Patient Passport, between 2014 and 2022, we conducted adjusted logistic regression (adjusting for year) and compared receipt of key items of care between those reporting that they had had an annual review (65.3%) and those who did not (34.%). To further capture patient experience, we also analyzed 4,228 free text responses to the 2021 Asthma + Lung UK annual COPD survey to the question “What’s the one thing that could improve your COPD care?”Results: We found that the absence of an annual review was associated with significantly worse COPD care across all domains studied, In particular inhaler training (Yes: 80.8% vs No: 38.4%, Adjusted Odds Ratio (AOR): 8.18 95% CI (7.89-8.47), having a written care plan (89.6% vs 56.9%, AOR 6.68 (6.35-7.05), and medication knowledge (72.6% vs 33.6%, AOR: 5.73 (5.51-5.96). Thematic analysis of the 2021 COPD survey responses identified three areas to improve care: 1) Access and support from healthcare services, 2) Improved treatment effectiveness, and 3) Interaction between COPD and the social environment.Discussion: Failure to deliver annual COPD reviews is associated with worse patient-reported experience of care quality. In parallel, people with COPD express a desire for greater support and access to healthcare services.
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Journal articleAgache I, Annesi-Maesano I, Cecchi L, et al., 2024,
EAACI guidelines on environmental science for allergy and asthma: The impact of short-term exposure to outdoor air pollutants on asthma-related outcomes and recommendations for mitigation measures
, ALLERGY, ISSN: 0105-4538 -
Journal articleKasetti P, Husain NF, Skinner TC, et al., 2024,
Personality traits and pre-treatment beliefs and cognitions predicting patient adherence to continuous positive airway pressure: A systematic review
, SLEEP MEDICINE REVIEWS, Vol: 74, ISSN: 1087-0792 -
Journal articlePham DD, Lee J-H, Kwon H-S, et al., 2024,
Prospective direct comparison of biologic treatments for severe eosinophilic asthma Findings from the PRISM study
, ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY, Vol: 132, Pages: 457-464, ISSN: 1081-1206
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