Imperial College London

ProfessorClareLloyd

Faculty of MedicineNational Heart & Lung Institute

Interim Head of NHLI, Vice-Dean (institutional Affairs) FoM
 
 
 
//

Contact

 

+44 (0)20 7594 3102c.lloyd Website

 
 
//

Location

 

Office 352Sir Alexander Fleming BuildingSouth Kensington Campus

//

Summary

 

Publications

Publication Type
Year
to

300 results found

Tian K, Dangarh P, Zhang H, Hines CL, Bush A, Pybus HJ, Harker JA, Lloyd CM, Tanaka RJ, Saglani Set al., 2024, Role of epithelial barrier function in inducing type 2 immunity following early-life viral infection., Clin Exp Allergy, Vol: 54, Pages: 109-119

BACKGROUND: Preschool wheeze attacks triggered by recurrent viral infections, including respiratory syncytial virus (RSV), are associated with an increased risk of childhood asthma. However, mechanisms that lead to asthma following early-life viral wheezing remain uncertain. METHODS: To investigate a causal relationship between early-life RSV infections and onset of type 2 immunity, we developed a neonatal murine model of recurrent RSV infection, in vivo and in silico, and evaluated the dynamical changes of altered airway barrier function and downstream immune responses, including eosinophilia, mucus secretion and type 2 immunity. RESULTS: RSV infection of neonatal BALB/c mice at 5 and 15 days of age induced robust airway eosinophilia, increased pulmonary CD4+ IL-13+ and CD4+ IL-5+ cells, elevated levels of IL-13 and IL-5 and increased airway mucus at 20 days of age. Increased bronchoalveolar lavage albumin levels, suggesting epithelial barrier damage, were present and persisted following the second RSV infection. Computational in silico simulations demonstrated that recurrent RSV infection resulted in severe damage of the airway barrier (epithelium), triggering the onset of type 2 immunity. The in silico results also demonstrated that recurrent infection is not always necessary for the development of type 2 immunity, which could also be triggered with single infection of high viral load or when the epithelial barrier repair is compromised. CONCLUSIONS: The neonatal murine model demonstrated that recurrent RSV infection in early life alters airway barrier function and promotes type 2 immunity. A causal relationship between airway barrier function and type 2 immunity was suggested using in silico model simulations.

Journal article

Joulia RPG, Puttur F, Stölting H, Traves W, Entwistle L, Voitovich A, Garcia Martín M, Al-Sahaf M, Bonner K, Scotney E, Molyneaux P, Hewitt R, Walker S, Yates L, Saglani S, Lloyd Cet al., 2024, Mast cell activation disrupts interactions between endothelial cells and pericytes during early life allergic asthma, Journal of Clinical Investigation, ISSN: 0021-9738

Journal article

O'Donnell V, Lloyd C, Tyrrell V, 2024, Correction., Allergy

Journal article

Hewitt R, Puttur F, Gaboriau D, Fercoq F, Fresquet M, Traves W, Yates LL, Walker S, Molyneaux P, Kemp S, Nicholson A, Rice A, Roberts E, Lennon R, Carlin L, Byrne A, Maher T, Lloyd Cet al., 2023, Lung extracellular matrix modulates KRT5+ basal cell activity in pulmonary fibrosis, Nature Communications, Vol: 14, ISSN: 2041-1723

Aberrant expansion of KRT5+ basal cells in the distal lung accompanies progressive alveolar epithelial cell loss and tissue remodelling during fibrogenesis in idiopathic pulmonary fibrosis (IPF). The mechanisms determining activity of KRT5+ cells in IPF have not been delineated. Here, we reveal a potential mechanism by which KRT5+ cells migrate within the fibrotic lung, navigating regional differences in collagen topography. In vitro, KRT5+ cell migratory characteristics and expression of remodelling genes are modulated by extracellular matrix (ECM) composition and organisation. Mass spectrometry- based proteomics revealed compositional differences in ECM components secreted by primary human lung fibroblasts (HLF) from IPF patients compared to controls. Over-expression of ECM glycoprotein, Secreted Protein Acidic and Cysteine Rich (SPARC) in the IPF HLF matrix restricts KRT5+ cell migration in vitro. Together, our findings demonstrate how changes to the ECM in IPF directly influence KRT5+ cell behaviour and function contributing to remodelling events in the fibrotic niche.

Journal article

Melen E, Lambrecht BN, Lloyd CM, Rothenberg ME, Kabashima K, Luciani F, Coquet JM, Ober C, Nawijn MC, Platts-Mills T, von Mutius Eet al., 2023, A conversation on allergy: recognizing the past and looking to the future, IMMUNOLOGY AND CELL BIOLOGY, ISSN: 0818-9641

Journal article

Lloyd CMM, Saglani S, 2023, Early-life respiratory infections and developmental immunity determine lifelong lung health, NATURE IMMUNOLOGY, ISSN: 1529-2908

Journal article

Granell R, Curtin JA, Haider S, Kitaba NT, Mathie SA, Gregory LG, Yates LL, Tutino M, Hankinson J, Perretti M, Vonk JM, Arshad HS, Cullinan P, Fontanella S, Roberts GC, Koppelman GH, Simpson A, Turner SW, Murray CS, Lloyd CM, Holloway JW, Custovic A, UNICORN and Breathing Together investigatorset al., 2023, A meta-analysis of genome-wide association studies of childhood wheezing phenotypes identifies ANXA1 as a susceptibility locus for persistent wheezing, eLife, Vol: 12, Pages: 1-57, ISSN: 2050-084X

BACKGROUND: Many genes associated with asthma explain only a fraction of its heritability. Most genome-wide association studies (GWASs) used a broad definition of 'doctor-diagnosed asthma', thereby diluting genetic signals by not considering asthma heterogeneity. The objective of our study was to identify genetic associates of childhood wheezing phenotypes. METHODS: We conducted a novel multivariate GWAS meta-analysis of wheezing phenotypes jointly derived using unbiased analysis of data collected from birth to 18 years in 9568 individuals from five UK birth cohorts. RESULTS: Forty-four independent SNPs were associated with early-onset persistent, 25 with pre-school remitting, 33 with mid-childhood remitting, and 32 with late-onset wheeze. We identified a novel locus on chr9q21.13 (close to annexin 1 [ANXA1], p<6.7 × 10-9), associated exclusively with early-onset persistent wheeze. We identified rs75260654 as the most likely causative single nucleotide polymorphism (SNP) using Promoter Capture Hi-C loops, and then showed that the risk allele (T) confers a reduction in ANXA1 expression. Finally, in a murine model of house dust mite (HDM)-induced allergic airway disease, we demonstrated that anxa1 protein expression increased and anxa1 mRNA was significantly induced in lung tissue following HDM exposure. Using anxa1-/- deficient mice, we showed that loss of anxa1 results in heightened airway hyperreactivity and Th2 inflammation upon allergen challenge. CONCLUSIONS: Targeting this pathway in persistent disease may represent an exciting therapeutic prospect. FUNDING: UK Medical Research Council Programme Grant MR/S025340/1 and the Wellcome Trust Strategic Award (108818/15/Z) provided most of the funding for this study.

Journal article

Harker JA, Lloyd CM, 2023, T helper 2 cells in asthma, JOURNAL OF EXPERIMENTAL MEDICINE, Vol: 220, ISSN: 0022-1007

Journal article

Saglani S, Yates L, Lloyd CM, 2023, Immunoregulation of asthma by type 2 cytokine therapies: Treatments for all ages?, EUROPEAN JOURNAL OF IMMUNOLOGY, ISSN: 0014-2980

Journal article

Puttur F, Lloyd CM, 2023, Breathing easy: Dopamine quenches the ILC2 flame, IMMUNITY, Vol: 56, Pages: 229-231, ISSN: 1074-7613

Journal article

Konstantinidi R, Yates LL, Saglani S, Lloyd CM, Patel AKet al., 2022, Investigating the influence of mRNA encoded transcription factor delivery on human bronchial epithelial cell differentiation, 29th Annual Congress of the European-Society-of-Gene-and-Cell-Therapy (ESCGT), Publisher: MARY ANN LIEBERT, INC, Pages: A194-A195, ISSN: 1043-0342

Conference paper

Pyle C, Patel D, Peiro T, Joulia R, Grabiec A, Hussell T, Tavernier G, Simpson A, Pease J, Harker J, Lloyd C, Snelgrove Ret al., 2022, MMP-12 supports pulmonary B cell follicle formation and local antibody responses during asthma, American Journal of Respiratory and Critical Care Medicine, Vol: 206, Pages: 1424-1428, ISSN: 1073-449X

Journal article

Albers GJ, Ogger PP, Gray R, Halket JM, Gauvreau G, O'Byrne P, Lloyd CM, Byrne AJet al., 2022, Allergen exposure induces airway macrophage metabolic reprogramming, Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936

Conference paper

Stolting H, Baillon L, Frise R, Bonner K, Hewitt RJ, Molyneaux PL, Gore ML, Barclay WS, Saglani S, Lloyd CMet al., 2022, Distinct airway epithelial immune responses after infection with SARS-CoV-2 compared to H1N1, Mucosal Immunology, Vol: 15, Pages: 952-963, ISSN: 1933-0219

Children are less likely than adults to suffer severe symptoms when infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), while influenza A H1N1 severity is comparable across ages except for the very young or elderly. Airway epithelial cells play a vital role in the early defence against viruses via their barrier and immune functions. We investigated viral replication and immune responses in SARS-CoV-2-infected bronchial epithelial cells from healthy paediatric (n = 6; 2.5–5.6 years old) and adult (n = 4; 47–63 years old) subjects and compared cellular responses following infection with SARS-CoV-2 or Influenza A H1N1. While infection with either virus triggered robust transcriptional interferon responses, including induction of type I (IFNB1) and type III (IFNL1) interferons, markedly lower levels of interferons and inflammatory proteins (IL-6, IL-8) were released following SARS-CoV-2 compared to H1N1 infection. Only H1N1 infection caused disruption of the epithelial layer. Interestingly, H1N1 infection resulted in sustained upregulation of SARS-CoV-2 entry factors FURIN and NRP1. We did not find any differences in the epithelial response to SARS-CoV-2 infection between paediatric and adult cells. Overall, SARS-CoV-2 had diminished potential to replicate, affect morphology and evoke immune responses in bronchial epithelial cells compared to H1N1.

Journal article

Stolting H, Lloyd CM, 2022, <i>Pseudomonas aeruginosa</i>: a pathogen making itself at home, TRENDS IN IMMUNOLOGY, Vol: 43, Pages: 497-499, ISSN: 1471-4906

Journal article

Rahimi RA, Cho JL, Jakubzick C, Khader SA, Lambrecht BN, Lloyd CM, Molofsky AB, Talbot S, Bonham CA, Drake WP, Sperling A, Singer BDet al., 2022, Advancing Lung Immunology Research An Official American Thoracic Society Workshop Report, AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, Vol: 67, Pages: E1-E18, ISSN: 1044-1549

Journal article

Salem V, Hirani D, Lloyd C, Regan L, Peters Cet al., 2022, Why are women still leaving academic medicine? A qualitative study within a London Medical School, BMJ Open, Vol: 12, ISSN: 2044-6055

Objectives: To identify factors that influenced women who chose to leave academic medicine.Design and main outcome measures: Independent consultants led a focus group of women in medicine who had left academia after completion of their postgraduate research degree at Imperial College London Faculty of Medicine. Thematic analysis was performed on the transcribed conversations.Participants and setting: Nine women physicians who completed a postgraduate degree (MD or PhD) at a large London Medical School and Academic Health Sciences Centre, Imperial College London, but did not go on to pursue a career in academic medicine.Results: Influences to leave clinical academia were summarised under eight themes—career intentions, supervisor support, institutional human resources support, inclusivity, work–life balance, expectations, mentors and role models, and pregnancy and maternity leave.Conclusion: The women in our focus group reported several factors contributing to their decision to leave clinical academia, which included lack of mentoring tailored to specific needs, low levels of acceptance for flexible working to help meet parental responsibilities and perceived explicit gender biases. We summarise the multiple targeted strategies that Imperial College London has implemented to promote retention of women in academic medicine, although more research needs to be done to ascertain the most effective interventions.

Journal article

Vijayakumar B, Boustani K, Ogger P, Papadaki A, Tonkin J, Orton C, Ghai P, Suveizdyte K, Hewitt R, Desai S, Devaraj A, Snelgrove R, Molyneaux P, Garner J, Peters J, Shah P, Lloyd C, Harker Jet al., 2022, Immuno-proteomic profiling reveals aberrant immune cell regulation in the airways of individuals with ongoing post-COVD-19 respiratory disease, Immunity, Vol: 55, Pages: 542-556.e5, ISSN: 1074-7613

Some patients hospitalized with acute COVID-19 suffer respiratory symptoms that persist for many months. We delineated the immune-proteomic landscape in the airway and peripheral blood of healthy controls and post-COVID-19 patients 3 to 6 months after hospital discharge. Post-COVID-19 patients showed abnormal airway (but not plasma) proteomes, with elevated concentration of proteins associated with apoptosis, tissue repair and epithelial injury versus healthy individuals. Increased numbers of cytotoxic lymphocytes were observed in individuals with greater airway dysfunction, while increased B cell numbers and altered monocyte subsets were associated with more widespread lung abnormalities. 1 year follow-up of some post-COVID-19 patients indicated that these abnormalities resolved over time. In summary, COVID-19 causes a prolonged change to the airway immune landscape in those with persistent lung disease, with evidence of cell death and tissue repair linked to ongoing activation of cytotoxic T cells.

Journal article

Starkey MR, Deshmukh H, Lukacs NW, Lloyd CMet al., 2022, Editorial: Pulmonary Innate Lymphoid Cells - Gatekeepers of Respiratory Health, FRONTIERS IN IMMUNOLOGY, Vol: 13, ISSN: 1664-3224

Journal article

Pattaroni C, Macowan M, Chatzis R, Daunt C, Custovic A, Shields MD, Power UF, Grigg J, Roberts G, Ghazal P, Schwarze J, Gore M, Turner S, Bush A, Saglani S, Lloyd C, Marsland BJet al., 2022, Early life inter-kingdom interactions shape the immunological environment of the airways, Microbiome, Vol: 10, ISSN: 2049-2618

Background: There is increasing evidence that the airway microbiome plays a key role in the establishment of respiratory health by interacting with the developing immune system early in life. While it has become clear that bacteria are involved in this process, there is a knowledge gap concerning the role of fungi. Moreover, the inter-kingdom interactions that influence immune development remain unknown. In this prospective exploratory human study, we aimed to determine early post-natal microbial and immunological features of the upper airways in 121 healthy newborns.Results: We found that the oropharynx and nasal cavity represent distinct ecological niches for bacteria and fungi. Breastfeeding correlated with changes in microbiota composition of oropharyngeal samples with the greatest impact upon the relative abundance of Streptococcus species and Candida. Host transcriptome profiling revealed that genes with the highest expression variation were immunological in nature. Multi-omics factor analysis of host and microbial data revealed unique co-variation patterns. Conclusion: These data provide evidence of a diverse multi-kingdom microbiota linked with local immunological characteristics in the first week of life that could represent distinct trajectories for future respiratory health.

Journal article

Pyle CJ, Labeur-Iurman L, Groves HT, Puttur F, Lloyd CM, Tregoning JS, Harker JAet al., 2021, Enhanced IL-2 in early life limits the development of TFH and protective antiviral immunity, Journal of Experimental Medicine, Vol: 218, ISSN: 0022-1007

T follicular helper cell (TFH)-dependent antibody responses are critical for long-term immunity. Antibody responses are diminished in early life, limiting long-term protective immunity and allowing prolonged or recurrent infection, which may be important for viral lung infections that are highly prevalent in infancy. In a murine model using respiratory syncytial virus (RSV), we show that TFH and the high-affinity antibody production they promote are vital for preventing disease on RSV reinfection. Following a secondary RSV infection, TFH-deficient mice had significantly exacerbated disease characterized by delayed viral clearance, increased weight loss, and immunopathology. TFH generation in early life was compromised by heightened IL-2 and STAT5 signaling in differentiating naive T cells. Neutralization of IL-2 during early-life RSV infection resulted in a TFH-dependent increase in antibody-mediated immunity and was sufficient to limit disease severity upon reinfection. These data demonstrate the importance of TFH in protection against recurrent RSV infection and highlight a mechanism by which this is suppressed in early life.

Journal article

McErlean P, Bell CG, Hewitt RJ, Busharat Z, Ogger PP, Ghai P, Albers GJ, Calamita E, Kingston S, Molyneaux PL, Beck S, Lloyd CM, Maher TM, Byrne AJet al., 2021, DNA methylome alterations are associated with airway macrophage differentiation and phenotype during lung fibrosis., American Journal of Respiratory and Critical Care Medicine, Vol: 204, Pages: 954-966, ISSN: 1073-449X

Rationale: Airway macrophages (AMs) are key regulators of the lung environment and are implicated in the pathogenesis of idiopathic pulmonary fibrosis (IPF), a fatal respiratory disease with no cure. However, knowledge about the epigenetics of AMs in IPF is limited. Objectives: To assess the role of epigenetic regulation of AMs during lung fibrosis. Methods: We undertook DNA methylation (DNAm) profiling by using Illumina EPIC (850k) arrays in sorted AMs from healthy donors (n = 14) and donors with IPF (n = 30). Cell-type deconvolution was performed by using reference myeloid-cell DNA methylomes. Measurements and Main Results: Our analysis revealed that epigenetic heterogeneity was a key characteristic of IPF AMs. DNAm "clock" analysis indicated that epigenetic alterations in IPF AMs were not associated with accelerated aging. In differential DNAm analysis, we identified numerous differentially methylated positions (n = 11) and differentially methylated regions (n = 49) between healthy and IPF AMs, respectively. Differentially methylated positions and differentially methylated regions encompassed genes involved in lipid (LPCAT1 [lysophosphatidylcholine acyltransferase 1]) and glucose (PFKFB3 [6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3]) metabolism, and importantly, the DNAm status was associated with disease severity in IPF. Conclusions: Collectively, our data identify that changes in the epigenome are associated with the development and function of AMs in the IPF lung.

Journal article

Helen S, Walker SA, Puttur F, Saglani S, Lloyd CMet al., 2021, LSC-2021-Epidermal growth factor receptor in airway remodelling during allergic airway disease - divergent roles during early life and adulthood?, Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936

Conference paper

Hewitt RJ, Lloyd CM, 2021, Regulation of immune responses by the airway epithelial cell landscape, NATURE REVIEWS IMMUNOLOGY, Vol: 21, Pages: 347-362, ISSN: 1474-1733

Journal article

Saglani S, Robinson P, Fontanella S, Ananth S, Martin Alonso A, Cook J, Kaya-de Vries D, Polo Silveira L, Gregory L, Lloyd C, Fleming L, Bush A, Custovic Aet al., 2021, Recurrent severe preschool wheeze: From pre-specified diagnostic labels to underlying endotypes, American Journal of Respiratory and Critical Care Medicine, Vol: 204, Pages: 523-535, ISSN: 1073-449X

Rationale: Preschool wheezing is heterogeneous, but the underlying mechanisms are poorly understood. Objectives: To investigate lower airway inflammation and infection in preschool children with different clinical diagnoses undergoing elective bronchoscopy/bronchoalveolar lavage-BAL. Methods: We recruited 136 children aged 1-5 years (105 recurrent severe wheeze-RSW; 31 non-wheeze respiratory disorders-NWRD). RSW were assigned as episodic viral-EVW or multiple trigger wheeze-MTW. We compared lower airway inflammation/infection in different clinical diagnoses and undertook data-driven analyses to determine clusters of pathophysiological features, and investigated their relationships with pre-specified diagnostic labels. Measurements and Main Results: Blood eosinophils and allergic sensitization were significantly higher in RSW than NWRD. Blood neutrophils, BAL eosinophils and neutrophils, and positive bacterial culture and virus detection rates were similar between groups. However, pathogen distribution differed significantly, with higher detection of rhinovirus in RSW and Moraxella in sensitized RSW. EVW and MTW did not differ in blood/BAL inflammation, or bacterial/virus detection. Partition Around Medoids algorithm revealed 4 clusters of pathophysiological features: (1) Atopic (17.9%); (2) Non-atopic, low infection rate, high inhaled corticosteroids-ICS (31.3%); (3) Non-atopic, high infection rate (23.1%); and (4) Non-atopic, low infection rate, no ICS (27.6%). Cluster allocation differed significantly between RSW and NWRD (RSW evenly distributed across clusters, 60% of NWRD assigned to cluster 4, p<0.001). There was no difference in cluster membership between EVW and MTW. Cluster 1 was dominated by Moraxella detection (p=0.04) and Cluster 3 by Haemophilus/Staphylococcus/ Streptococcus (p=0.02). Conclusions: We identified four clusters of severe preschool wheeze distinguished using sensitization, peripheral eosinophilia, lower airway neutrophilia and bacteriolog

Journal article

Branchett WJ, Cook J, Oliver RA, Bruno N, Walker SA, Stӧlting H, Mack M, OGarra A, Saglani S, Lloyd CMet al., 2021, Airway macrophage-intrinsic TGF-β1 regulates pulmonary immunity during early life allergen exposure, Journal of Allergy and Clinical Immunology, Vol: 147, Pages: 1892-1906, ISSN: 0091-6749

BackgroundEarly life represents a major risk window for asthma development. However, the mechanisms controlling the threshold for establishment of allergic airway inflammation in early life are incompletely understood. Airway macrophages (AMs) regulate pulmonary allergic responses and undergo TGF-β–dependent postnatal development, but the role of AM maturation factors such as TGF-β in controlling the threshold for pathogenic immune responses to inhaled allergens remains unclear.ObjectiveOur aim was to test the hypothesis that AM-derived TGF-β1 regulates pathogenic immunity to inhaled allergen in early life.MethodsConditional knockout (Tgfb1ΔCD11c) mice, with TGF-β1 deficiency in AMs and other CD11c+ cells, were analyzed throughout early life and following neonatal house dust mite (HDM) inhalation. The roles of specific chemokine receptors were determined by using in vivo blocking antibodies.ResultsAM-intrinsic TGF-β1 was redundant for initial population of the neonatal lung with AMs, but AMs from Tgfb1ΔCD11c mice failed to adopt a mature homeostatic AM phenotype in the first weeks of life. Evidence of constitutive TGF-β1 signaling was also observed in pediatric human AMs. TGF-β1–deficient AMs expressed enhanced levels of monocyte-attractant chemokines, and accordingly, Tgfb1ΔCD11c mice exposed to HDM throughout early life accumulated CCR2-dependent inflammatory CD11c+ mononuclear phagocytes into the airway niche that expressed the proallergic chemokine CCL8. Tgfb1ΔCD11c mice displayed augmented TH2, group 2 innate lymphoid cell, and airway remodeling responses to HDM, which were ameliorated by blockade of the CCL8 receptor CCR8.ConclusionOur results highlight a causal relationship between AM maturity, chemokines, and pathogenic immunity to environmental stimuli in early life and identify TGF-β1 as a key regulator of this.

Journal article

Harker JA, Lloyd CM, 2021, Overlapping and distinct features of viral and allergen immunity in the human lung, IMMUNITY, Vol: 54, Pages: 617-631, ISSN: 1074-7613

Journal article

Albers GJ, Iwasaki J, McErlean P, Ogger PP, Ghai P, Khoyratty TE, Udalova IA, Lloyd CM, Byrne AJet al., 2021, IRF5 regulates airway macrophage metabolic responses, CLINICAL AND EXPERIMENTAL IMMUNOLOGY, Vol: 204, Pages: 134-143, ISSN: 0009-9104

Journal article

Invernizzi R, Wu BG, Barnett J, Ghai P, Kingston S, Hewitt RJ, Feary J, Li Y, Chua F, Wu Z, Wells AU, Renzoni EA, Nicholson AG, Rice A, Devaraj A, Segal LN, Byrne AJ, Maher TM, Lloyd CM, Molyneaux PLet al., 2021, The respiratory microbiome in chronic hypersensitivity pneumonitis is distinct from that of idiopathic pulmonary fibrosis, American Journal of Respiratory and Critical Care Medicine, Vol: 203, Pages: 339-347, ISSN: 1073-449X

RATIONALE: Chronic hypersensitivity pneumonitis (CHP) is a condition that arises following repeated exposure and sensitisation to inhaled antigens. The lung microbiome is increasingly implicated in respiratory disease but to date, no study has investigated the composition of microbial communities in the lower airways in CHP. OBJECTIVE: To characterise and compare the airway microbiome in subjects with CHP, idiopathic pulmonary fibrosis (IPF) and controls. METHODS: We prospectively recruited individuals diagnosed with CHP (n=110), IPF (n=45) and controls (n=28). Subjects underwent bronchoalveolar lavage and bacterial DNA was isolated, quantified by qPCR and the 16S rRNA gene was sequenced to characterise the bacterial communities in the lower airways. MAIN MEASUREMENTS AND RESULTS: Distinct differences in the microbial profiles were evident in the lower airways of subjects with CHP and IPF. At the phylum level, the prevailing microbiota of both IPF and CHP subjects included Firmicutes, Bacteroidetes, Proteobacteria and Actinobacteria. However, in IPF, Firmicutes dominated while the percentage of reads assigned to Proteobacteria in the same group was significantly lower compared to CHP subjects. At the genus level, Staphylococcus was increased in CHP and Actinomyces and Veillonella in IPF. The lower airway bacterial burden in CHP subjects was higher than controls but lower than those with IPF. In contrast to IPF, there was no association between bacterial burden and survival in CHP. CONCLUSIONS: The microbial profile of the lower airways in subjects with CHP is distinct from that of IPF and, notably, bacterial burden in individuals with CHP fails to predict survival.

Journal article

Invernizzi R, Giallourou N, Swann JR, Hewitt RJ, Ghai P, Wu BG, Li Y, Segal LN, Byrne AJ, Maher TM, Lloyd CM, Molyneaux PLet al., 2021, THE RESPIRATORY MICROBIOME AND METABOLOME IN IDIOPATHIC PULMONARY FIBROSIS, Publisher: BMJ PUBLISHING GROUP, Pages: A2-A3, ISSN: 0040-6376

Conference paper

This data is extracted from the Web of Science and reproduced under a licence from Thomson Reuters. You may not copy or re-distribute this data in whole or in part without the written consent of the Science business of Thomson Reuters.

Request URL: http://wlsprd.imperial.ac.uk:80/respub/WEB-INF/jsp/search-html.jsp Request URI: /respub/WEB-INF/jsp/search-html.jsp Query String: respub-action=search.html&id=00303622&limit=30&person=true