Divya Mohan

Indian Veterinary Research Institute

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Michael I. Polkey

Royal Brompton & Harefield NHS Foundation Trust

Ruth Tal‐Singer

COPD Foundation

Ian B. Wilkinson

University of Cambridge

Marie Fisk

Cambridge University Hospitals NHS Foundation Trust

Carmel M. McEniery

University of Cambridge

Joseph Cheriyan

Cambridge University Hospitals NHS Foundation Trust

Charlotte E. Bolton

University of Nottingham

William MacNee

University of Edinburgh

Jonathan Fuld

Cambridge University Hospitals NHS Foundation Trust

John Cockcroft

Cardiff Metropolitan University

Cooperative Institutions

Imperial College London

Indian Veterinary Research Institute

Royal Brompton & Harefield NHS Foundation Trust

University of Cambridge

Central Drug Research Institute

GlaxoSmithKline (United Kingdom)

National Institute for Health Research

Addenbrooke's Hospital

University College London

Cambridge University Hospitals NHS Foundation Trust

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Systemic inflammation in COPD : effects on skeletal muscle and the cardiovascular system

Divya Mohan

10.25560/55255

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Elevated QRISK2 score in patients hospitalized for acute exacerbation of COPD versus stable COPD outpatients

International Journal of Cardiology (2014)

Elisa Pagliaroli Divya Mohan V Padmanaban Paolo Palange Sarah Elkin

10.1016/j.ijcard.2014.11.065

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Protein Expression Differences of 2‐Dimensional and Progressive 3‐Dimensional Cell Cultures of Non‐Small‐Cell‐Lung‐Cancer Cell Line H460

Journal of Cellular Biochemistry (2016)

Maddaly Ravi Divya Mohan Bellona Sahu

Non-small-cell-lung-cancer (NSCLC) constitutes about 75-80% of lung cancers. The challenge to tackle cancers is in early diagnosis and arriving at safer therapeutic options. In vitro studies using cancer cell lines continue to contribute significantly in understanding cancers. Cell culture methods have evolved and the recent developments in 3 dimensional (3D) cell cultures are inducing greater resemblance of the in vitro cultured cells with in vivo conditions. In this study, we established 3D aggregates of H460 cell line on agarose hydrogels and studied the protein expression differences among cells grown as monolayers (2D) and the progressively developing 3D aggregates from days 2 to 10. Analysis included matching of those proteins expressed by the developing aggregates and the available literature on progressing tumors in vivo. J. Cell. Biochem. 118: 1648-1652, 2017. © 2016 Wiley Periodicals, Inc.

3D cell culture

10.1002/jcb.25800

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Evaluation of anti-hypertensive activity of Ulmus wallichiana extract and fraction in SHR, DOCA-salt- and L-NAME-induced hypertensive rats

Journal of Ethnopharmacology (2016)

Syed Anees Ahmed Shibani Lahiri Divya Mohan Guru R. Valicherla Anand P. Gupta

Spontaneously hypertensive rat

Folk medicine

10.1016/j.jep.2016.10.008

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Cardioprotective Effect of Ulmus wallichiana Planchon in β-Adrenergic Agonist Induced Cardiac Hypertrophy

Frontiers in Pharmacology (2016)

Syed Anees Ahmed Shibani Lahiri Divya Mohan Guru R. Valicherla Anand P. Gupta

Ulmus wallichiana Planchon (Family: Ulmaceae), a traditional medicinal plant, was used in fracture healing in the folk tradition of Uttarakhand, Himalaya, India. The present study investigated the cardioprotective effect of ethanolic extract (EE) and butanolic fraction (BF) of U. wallichiana in isoprenaline (ISO) induced cardiac hypertrophy in Wistar rats. Cardiac hypertrophy was induced by ISO (5 mg/kg/day, subcutaneously) in rats. Treatment was performed by oral administration of EE and BF of U. wallichiana (500 mg/kg/day and 50 mg/kg/day). The blood pressure (BP) and heart rate (HR) were measured by non-invasive blood pressure (NIBP) measurement technique. Plasma renin, Ang II, NO and cGMP level were estimated using an ELISA kit. ACE activity was estimated. Blood pressure and heart rate were significantly increased in ISO group (130.33± 1.67 mmHg vs 111.78±1.62 mmHg, p<0.001 and 450.51±4.90 beats/min vs 347.82±6.91 beats/min respectively, p<0.001). The BP and HR were significantly reduced (EE: 117.53±2.27 mmHg vs 130.33±1.67 mmHg, p<0.001, BF: 119.74±3.32 mmHg vs 130.33±1.67 mmHg, p<0.001); HR: (EE: 390.22±8.24 beats/min vs 450.51±4.90 beats/min, p<0.001, BF: 345.38±6.79 beats/min vs 450.51±4.90 beats/min, p<0.001) after the treatment of EE and BF of U. wallichiana, respectively. Plasma renin, Ang II, ACE activity was decreased and NO, cGMP level were increased. The EE and BF of U. wallichiana down regulated the expression of ANP, BNP, TNF-α, IL-6, MMP9, β1 AR,TGFβ1 and up regulated NOS3, ACE2 and Mas expression level respectively. Thus, this study demonstrated that U. wallichiana has cardioprotective effect against ISO induced cardiac hypertrophy.

Isoprenaline

10.3389/fphar.2016.00510

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DEFINING THE FREQUENT EXACERBATOR PHENOTYPE DURING A PANDEMIC IN COPD

CHEST Journal (2021)

Parul Dayal Colin Dimond Xiaoying Yang Matthew Kent Shemra Rizzo

Copd exacerbation

Pandemic

10.1016/j.chest.2021.07.1622

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Risk assessment for hospital admission in patients with COPD; a multi-centre UK prospective observational study

PLoS ONE (2020)

Jilles M. Fermont Charlotte E. Bolton Marie Fisk Divya Mohan William MacNee

In chronic obstructive pulmonary disease (COPD), acute exacerbation of COPD requiring hospital admission is associated with mortality and healthcare costs. The ERICA study assessed multiple clinical measures in people with COPD, including the short physical performance battery (SPPB), a simple test of physical function with 3 components (gait speed, balance and sit-to-stand). We tested the hypothesis that SPPB score would relate to risk of hospital admissions and length of hospital stay. Data were analysed from 714 of the total 729 participants (434 men and 280 women) with COPD. Data from this prospective observational longitudinal study were obtained from 4 secondary and 1 tertiary centres from England, Scotland, and Wales. The main outcome measures were to estimate the risk of hospitalisation with acute exacerbation of COPD (AECOPD and length of hospital stay derived from hospital episode statistics (HES). In total, 291 of 714 individuals experienced 762 hospitalised AECOPD during five-year follow up. Poorer performance of SPPB was associated with both higher rate (IRR 1.08 per 1 point decrease, 95% CI 1.01 to 1.14) and increased length of stay (IRR 1.18 per 1 point decrease, 95% CI 1.10 to 1.27) for hospitalised AECOPD. For the individual sit-to-stand component of the SPPB, the association was even stronger (IRR 1.14, 95% CI 1.02 to 1.26 for rate and IRR 1.32, 95% CI 1.16 to 1.49 for length of stay for hospitalised AECOPD). The SPPB, and in particular the sit-to-stand component can both evaluate the risk of H-AECOPD and length of hospital stay in COPD. The SPPB can aid in clinical decision making and when prioritising healthcare resources.

Rate ratio

10.1371/journal.pone.0228940

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Quantitative analysis of dynamic 18F-FDG in lungs of HV and COPD subjects

Christopher Coello Marie Fisk Fred Wilson Divya Mohan Andy Brown

482 Objectives An inflammatory reaction in the airways and lung parenchyma, comprised mainly of neutrophils and alveolar macrophages is present in some patients with Chronic Obstructive Pulmonary Disease (COPD). Thoracic 18F-FDG PET/CT has been proposed as a promising imaging biomarker to assess inflammation [1,2,3]. We sought to assess the hypothesis that COPD subjects with evidence of circulating inflammation (i.e. elevated circulating fibrinogen) have a higher metabolic rate of 18F-FDG in lung parenchyma compared to healthy volunteers (HV). The metabolic rate of 18F-FDG uptake was measured using a novel fully quantitative approach via a kinetic model which derives the radioactivity signal from tissue only, applying correction for blood and air components of a region of interest. Methods The project received ethical committee approval and written informed consent was obtained from all participants. Sixty-nine high-fibrinogen (>2.8g/l) COPD (NCT01541852, funding: Technology Strategy Board (9157-61188)) and 10 never smoking HV were dynamically scanned for 60 min following bolus injection of 18F-FDG. CT-AC images were used to delineate regions of interest (ROIs) for the whole lung (WL) and upper, middle and lower subdivisions (UL, ML and LL) of the lung. These ROIs were applied to the dynamic FBP reconstructed PET data to extract regional time activity curves. Fraction of air (VaCT) in the ROI was estimated from the CT-AC image and included in expression of the measured FDG uptake: Cmeas(t) = Vb × CWB(t) + (1-Vb-VaCT) × CT(t,K1,k2,k3,CWB). The metabolic rate (MR) of 18F-FDG (Kiabc=K1k3/(k2+k3)) and the fraction of blood (Vbabc) for each ROI were estimated using an irreversible two-tissue compartmental model to describe the parenchyma kinetics (CT(t)). Patlak graphical analysis with normalisation to the intercept (nKiPat) were generated by dividing the slope by the intercept to enable comparison with previous published work [1,2,3]. Normalisation by the intercept (VssPat, the steady state volume of distribution of non-phosphorylated 18F-FDG) has previously been proposed as a way of correcting for the air component [1]. Effect size was estimated using Hedge’s g metric. Results In the whole lung, no difference (Figure 1, right, g=0.19[-0.48 0.86]) in the MR of 18F-FDG in tissue between HV (N=10, Kiabc=5.9±1.9x10-3 ml.cm-3.min-1) and COPD (N=69, Kiabc =5.4±2.6x10-3 ml.cm-3.min-1) was observed whereas a difference (g=-0.86[-1.56 -0.20]) was observed with Patlak graphical analysis (N=10, nKiPat=2.8±0.4x10-3 ml.cm-3.min-1) and COPD (N=69, nKiPat =5.4±2.6x10-3 ml.cm-3.min-1). nKiPat estimates were similar to those reported previously (Table 1). Group difference observed with nKiPat is driven by the Patlak intercept (Figure 2, left) which is not just dependent on the amount of air but also the amount of blood (Figure 2, right) in the ROI making VssPat an invalid surrogate for the correction of the air volume. Conclusions The lack of difference in the MR of 18F-FDG between systemic inflamed COPD and HVs suggests that 18F-FDG is not an appropriate biomarker for detecting inflammation in this patient group. Investigation of focal regions or alternate populations will be required in order to understand whether 18F-FDG has more general utility for imaging lung parenchyma inflammation but our data suggest other more specific tracers of the inflammatory process are required. [1] Jones et al. doi 10.1183/09031936.03.00048502 [2] Chen et al. doi 10.1164/ajrccm-conference.2011.183.1_MeetingAbstracts.A6449 [3] Subramanian et al. doi 10.1164/rccm.201201-0051OC Figure 1. Group comparison between HV and COPD with nKiPat (left) and Kiabc (right). AGM: age and gender matched.Figure 2. LEFT: Patlak intercept difference in WL. RIGHT: Scatter plot representing the intercept of Patlak and the blood volume estimated. Squares: HV, circles: COPD. $$graphic_3664FB65-1497-4DC4-A538-2F9CF74A939F$$ Figure 2. LEFT: Patlak intercept difference in WL. RIGHT: Scatter plot representing the intercept of Patlak and the blood volume estimated. Squares: HV, circles: COPD. $$graphic_AF7321CB-9AAE-43C7-8EAF-5466D342DA25$$

Parenchyma

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Late Breaking Abstract - Co-morbid disease clusters in chronic obstructive pulmonary disease: the ERICA study

01.02 - Rehabilitation and chronic care (2017)

Divya Mohan Matthew Allinder Julia Forman Carmel M. McEniery Charlotte E. Bolton

Background: Comorbidities are common in Chronic Obstructive Pulmonary Disease (COPD), related to heterogeneity, morbidity and mortality. We aimed to identify disease clusters to examine overlap of extra-pulmonary manifestations in COPD. Methods: 729 GOLD II–IV COPD subjects underwent multiple phenotypic assessments, including aortic pulse wave velocity (aPWV) and isometric quadriceps strength, in a prospective, observational study. Baseline data was subject to k-means cluster analysis. Results: Four phenotypic clusters emerged: subjects with systemic inflammation, moderate airflow obstruction and frequent exacerbations (cluster 1), subjects without systemic inflammation but severe airflow obstruction (cluster 2), subjects with moderate airflow obstruction and vascular comorbidities (cluster 3) and fewer comorbidities (cluster 4). Elevated aPWV and muscle weakness were present across clusters 1, 2 and 3, yet functional and patient reported measures were worst within clusters 1 and 3. Conclusions: Distinct clusters of COPD identified in the ERICA cohort demonstrated that airflow limitation alone cannot predict the presence of extrapulmonary manifestations, vascular risks or functional limitation. ERICA was funded by a grant from Innovate UK and contributions in kind from GSK.

10.1183/1393003.congress-2017.oa4664

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ALIENTO and ARNASA: Study designs of two randomised, double-blind, placebo-controlled trials of astegolimab in patients with COPD

05.01 - Airway pharmacology and treatment (2023)

Christopher E. Brightling James D. Chalmers Parameswaran Nair Neil Greening Russell P. Bowler

Rationale: The interleukin (IL)-33/ST2 pathway is linked to COPD exacerbations. Astegolimab, a human IgG2 monoclonal antibody, inhibits the IL-33 receptor ST2, is well tolerated and may reduce COPD exacerbations. Here, we report the study designs of the Phase IIb ALIENTO (NCT05037929) and Phase III ARNASA (NCT05595642) trials investigating the efficacy and safety of astegolimab in patients with COPD. Methods: ALIENTO and ARNASA are randomised, double-blind, placebo-controlled multicentre trials. In each trial, ~1290 patients will be enrolled and randomised (1:1:1) to receive astegolimab every 2 or every 4 weeks or placebo. Both trials will consist of a 52-week placebo-controlled period, followed by a 12-week safety follow-up period for patients who do not enter the OLE. Eligible patients must be aged 40–90 (ALIENTO) or 40–80 (ARNASA) years, former or current smokers, have a COPD diagnosis ≥12 months prior to screening and have experienced ≥2 moderate or severe exacerbations within 12 months prior to screening. Patients must have post-bronchodilator percent predicted FEV₁ ≥20‒<80% and FEV₁/FVC <0.7 at screening (ALIENTO) or at Visit 1 or 2 (ARNASA). The primary endpoint for both trials is the annualised rate of moderate and severe COPD exacerbations from baseline to Week 52. Secondary endpoints include: time to first moderate or severe COPD exacerbation; patient-reported outcomes (St. George9s Respiratory Questionnaire-COPD, Evaluating Respiratory Symptoms in COPD); and change from baseline in post-bronchodilator FEV₁ at Week 52. Conclusions: ALIENTO and ARNASA aim to establish the efficacy and safety of astegolimab in the treatment of patients with COPD.

Clinical endpoint

10.1183/13993003.congress-2023.pa1292

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