A5065757644- Asthma and respiratory diseases
- Respiratory and Cough-Related Research
- Chronic Obstructive Pulmonary Disease (COPD) Research
- Eosinophilic Esophagitis
- IL-33, ST2, and ILC Pathways
- Neuropeptides and Animal Physiology
- Inhalation and Respiratory Drug Delivery
- Neonatal Respiratory Health Research
- Receptor Mechanisms and Signaling
- Eosinophilic Disorders and Syndromes
- Pediatric health and respiratory diseases
- Allergic Rhinitis and Sensitization
- Immune cells in cancer
- Airway Management and Intubation Techniques
- Ion Channels and Receptors
- Analytical Methods in Pharmaceuticals
- Congenital Heart Disease Studies
- Bioactive Natural Diterpenoids Research
- Cancer, Stress, Anesthesia, and Immune Response
- Inflammation biomarkers and pathways
- Drug-Induced Hepatotoxicity and Protection
- Venomous Animal Envenomation and Studies
- Lung Cancer Treatments and Mutations
- Inflammatory mediators and NSAID effects
- Medical Coding and Health Information
University of Leicester
2013-2020
Sudan Academy of Sciences
2020
NIHR Leicester Biomedical Research Centre
2014-2018
Glenfield Hospital
2013-2016
University Hospitals of Leicester NHS Trust
2014
University of Suffolk
2013
Medina General Hospital
1995
Mast cell localization within the airway smooth muscle (ASM)-bundle plays an important role in development of hyper-responsiveness (AHR). Genomewide association studies implicate 'alarmin' IL-33 asthma, but its mast cell-ASM interactions is unknown.We examined expression and functional bronchial biopsies patients with without ex vivo ASM, cells, cocultured cells a mouse model system.IL-33 protein was assessed human tissue from 9 healthy controls, 18 mild-to-moderate 12 severe asthmatic by...
Cellular and computational models bronchial biopsies from asthma patients show that a DP 2 antagonist reduces airway smooth muscle mass in asthma.
Bronchial thermoplasty is a treatment for asthma. It currently unclear whether its histopathological impact sufficiently explained by the proportion of airway wall that exposed to temperatures necessary affect cell survival.Airway smooth muscle and bronchial epithelial cells were media (37-70°C) 10 s mimic thermoplasty. In silico we developed mathematical model heat distribution post-thermoplasty. vivo determined mass integrity pre- post-thermoplasty in 14 patients with severe asthma.In...
Airway remodelling in asthma remains poorly understood. This study aimed to determine the association of airway measured on bronchial biopsies with 1) lung function impairment and 2) thoracic quantitative computed tomography (QCT)-derived morphometry densitometry measures proximal air trapping. Subjects were recruited from a single centre. Bronchial biopsy features that strongest predictors QCT-derived trapping markers determined by stepwise multiple regression. The best predictor was...
In recent years, asthma has been defined primarily as an inflammatory disorder with emphasis on inflammation being the principle underlying pathophysiological characteristic driving airway obstruction and remodelling. Morphological abnormalities of asthmatic smooth muscle (ASM), primary structure responsible for seen in asthma, have long described, but surprisingly, until recently, relatively small number studies investigated whether ASM was also fundamentally different its functional...
There is evidence supporting a role for the nociceptin/orphanin FQ (N/OFQ; NOP) receptor and its endogenous ligand N/OFQ in modulation of neurogenic inflammation, airway tone calibre. We hypothesized that NOP activation has beneficial effects upon asthma immunopathology hyperresponsiveness. Therefore, expression function were examined healthy asthmatic human tissues. The concept was further addressed an animal model allergic asthma.NOP investigated by quantitative real-time PCR. Sputum...
The role of fibrocytes in chronic obstructive pulmonary disease (COPD) is unknown. We sought to enumerate blood and tissue COPD determine the association with clinical features disease.Utilizing flow cytometry identify circulating, collagen type 1+ cells, we found two populations: (i) CD45+ CD34+ (fibrocytes) (ii) CD34- [myeloid-derived suppressor cell (MDSC)-like fibrocytes] cells stable (n = 41) control 29) subjects. Lung resection material from a separate group subjects 11) or without was...
Abstract Objectives Airway hyper‐responsiveness and persistent airflow obstruction contribute to asthma pathogenesis symptoms, due in part airway smooth muscle (ASM) hypercontractility increased ASM mass. Fibrocytes have been shown localise the however it is not known whether fibrocytes nonasthmatic eosinophilic bronchitis (NAEB) chronic obstructive pulmonary disease (COPD). In addition, potential consequences of fibrocyte localisation as regards pathophysiology has widely studied. Methods...
The bronchial epithelium contributes to airway remodeling in asthma. DP2/CRTh2 is expressed by intact epithelium, and its stimulation <i>in vitro</i> increases epithelial cell migration metaplasia which are inhibited CRTh2 antagonism. This study investigated the effects of QAW039, an oral antagonist on integrity asthmatics with treatment-resistant sputum eosinophilia. Asthmatic subjects (GINA II-V) a ≥2% baseline eosinophil count were randomized QAW039 225mg BID or placebo addition their...
<b>Background:</b> Bronchial Thermoplasty (BT) has been shown to improve asthma control and symptoms, reduce exacerbation frequency rescue medication use. Small studies have reduced airway smooth muscle (ASM) mass following BT, but understanding of the mechanism action BT is incomplete. <b>Aims:</b> To investigate clinical, physiological histological effects in severe asthma. <b>Methods:</b> 34 patients undergoing as part clinical care were recruited from four UK centres. Asthma...
<h3>Introduction and objectives</h3> Oxidative stress has been implicated in the pathogenesis of asthma. Validated sputum biomarkers are required to assess this its relationship other clinical variables. We sought compare bronchial 8-oxodG expression asthma health; repeatability; explore with induced inflammatory cells counts exacerbations. <h3>Methods</h3> Asthmatics healthy controls were recruited from a single centre underwent characterisation including induction (asthma n = 58, health...
Activation of the DP2/CRTh2 receptor by prostaglandin D2 (PGD2) in airway mediates pro-inflammatory responses from immune cells and epithelial remodelling. The smooth muscle (ASM) is dysfunctional asthma with an increase mass infiltration mast which release PGD2 following allergen challenge. role PGD2/CRTh2 axis ASM has not been studied extensively. Expression function CRTh2 primary asthmatics was assessed flow cytometry, migration a wound healing assay, F-actin content phalloidin...