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Article ; Online: T regulatory cells from atopic asthmatic individuals show a Th2-like phenotype.

Jansen, Kirstin / Satitsuksanoa, Pattraporn / Wirz, Oliver F / Schneider, Stephan R / van de Veen, Willem / Tan, Ge / Sokolowska, Milena / Message, Simon D / Kebadze, Tatiana / Glanville, Nicholas / Mallia, Patrick / Akdis, Cezmi A / Moniuszko, Marcin / Johnston, Sebastian L / Nadeau, Kari / Akdis, Mübeccel

Allergy

2021 Volume 77, Issue 4, Page(s) 1320–1324

MeSH term(s)	Asthma ; Humans ; Hypersensitivity, Immediate ; Phenotype ; Th2 Cells
Language	English
Publishing date	2021-12-11
Publishing country	Denmark
Document type	Letter ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	391933-x
ISSN	1398-9995 ; 0105-4538
ISSN (online)	1398-9995
ISSN	0105-4538
DOI	10.1111/all.15193
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Article ; Online: Experimental rhinovirus infection induces an antiviral response in circulating B cells which is dysregulated in patients with asthma.

Wirz, Oliver F / Jansen, Kirstin / Satitsuksanoa, Pattraporn / van de Veen, Willem / Tan, Ge / Sokolowska, Milena / Mirer, David / Stanić, Barbara / Message, Simon D / Kebadze, Tatiana / Glanville, Nicholas / Mallia, Patrick / Gern, James E / Papadopoulos, Nikolaos / Akdis, Cezmi A / Johnston, Sebastian L / Nadeau, Kari / Akdis, Mübeccel

Allergy

2021 Volume 77, Issue 1, Page(s) 130–142

Abstract: Background: Rhinoviruses are the predominant cause of respiratory viral infections and are strongly associated with asthma exacerbations. While humoral immunity plays an important role during virus infections, cellular aspects of this response are less ... ...

Abstract	Background: Rhinoviruses are the predominant cause of respiratory viral infections and are strongly associated with asthma exacerbations. While humoral immunity plays an important role during virus infections, cellular aspects of this response are less well understood. Here, we investigated the antiviral response of circulating B cells upon experimental rhinovirus infection in healthy individuals and asthma patients. Methods: We purified B cells from experimentally infected healthy individuals and patients with asthma and subjected them to total RNA-sequencing. Rhinovirus-derived RNA was measured in isolated B cells using a highly sensitive PCR. B cells were stimulated with rhinovirus in vitro to further study gene expression, expression of antiviral proteins and B-cell differentiation in response rhinovirus stimulation. Protein expression of pro-inflammatory cytokines in response to rhinovirus was assessed using a proximity extension assay. Results: B cells isolated from experimentally infected subjects exhibited an antiviral gene profile linked to IFN-alpha, carried viral RNA in vivo and were transiently infected by rhinovirus in vitro. B cells rapidly differentiated into plasmablasts upon rhinovirus stimulation. While B cells lacked expression of interferons in response to rhinovirus exposure, co-stimulation with rhinovirus and IFN-alpha upregulated pro-inflammatory cytokine expression suggesting a potential new function of B cells during virus infections. Asthma patients showed extensive upregulation and dysregulation of antiviral gene expression. Conclusion: These findings add to the understanding of systemic effects of rhinovirus infections on B-cell responses in the periphery, show potential dysregulation in patients with asthma and might also have implications during infection with other respiratory viruses.
MeSH term(s)	Antiviral Agents/therapeutic use ; Asthma ; Cytokines/pharmacology ; Humans ; Interferons ; Picornaviridae Infections ; Rhinovirus
Chemical Substances	Antiviral Agents ; Cytokines ; Interferons (9008-11-1)
Language	English
Publishing date	2021-07-16
Publishing country	Denmark
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	391933-x
ISSN	1398-9995 ; 0105-4538
ISSN (online)	1398-9995
ISSN	0105-4538
DOI	10.1111/all.14985
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Article ; Online: Bronchial mucosal inflammation and illness severity in response to experimental rhinovirus infection in COPD.

Zhu, Jie / Mallia, Patrick / Footitt, Joseph / Qiu, Yusheng / Message, Simon D / Kebadze, Tatiana / Aniscenko, Julia / Barnes, Peter J / Adcock, Ian M / Kon, Onn M / Johnson, Malcolm / Contoli, Marco / Stanciu, Luminita A / Papi, Alberto / Jeffery, Peter K / Johnston, Sebastian L

The Journal of allergy and clinical immunology

2020 Volume 146, Issue 4, Page(s) 840–850.e7

Abstract: Background: Respiratory viral infection causes chronic obstructive pulmonary disease (COPD) exacerbations. We previously reported increased bronchial mucosa eosinophil and neutrophil inflammation in patients with COPD experiencing naturally occurring ... ...

Abstract	Background: Respiratory viral infection causes chronic obstructive pulmonary disease (COPD) exacerbations. We previously reported increased bronchial mucosa eosinophil and neutrophil inflammation in patients with COPD experiencing naturally occurring exacerbations. But it is unclear whether virus per se induces bronchial mucosal inflammation, nor whether this relates to exacerbation severity. Objectives: We sought to determine the extent and nature of bronchial mucosal inflammation following experimental rhinovirus (RV)-16-induced COPD exacerbations and its relationship to disease severity. Methods: Bronchial mucosal inflammatory cell phenotypes were determined at preinfection baseline and following experimental RV infection in 17 Global Initiative for Chronic Obstructive Lung Disease stage II subjects with COPD and as controls 20 smokers and 11 nonsmokers with normal lung function. No subject had a history of asthma/allergic rhinitis: all had negative results for aeroallergen skin prick tests. Results: RV infection increased the numbers of bronchial mucosal eosinophils and neutrophils only in COPD and CD8 Conclusions: Experimental RV infection induces bronchial mucosal eosinophilia and neutrophilia only in patients with COPD and monocytes/macrophages and lymphocytes in both patients with COPD and control subjects. The virus-induced inflammatory cell phenotypes observed in COPD positively related to virus load and illness severity. Antiviral/anti-inflammatory therapies could attenuate bronchial inflammation and ameliorate virus-induced COPD exacerbations.
MeSH term(s)	B-Lymphocyte Subsets/immunology ; B-Lymphocyte Subsets/metabolism ; Biomarkers ; Eosinophils ; Female ; Humans ; Inflammation Mediators ; Leukocyte Count ; Male ; Neutrophils ; Picornaviridae Infections/complications ; Picornaviridae Infections/diagnosis ; Picornaviridae Infections/virology ; Pulmonary Disease, Chronic Obstructive/complications ; Pulmonary Disease, Chronic Obstructive/diagnosis ; Respiratory Function Tests ; Respiratory Mucosa/pathology ; Respiratory Mucosa/virology ; Rhinovirus ; Severity of Illness Index ; Sputum/cytology ; Sputum/metabolism ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism
Chemical Substances	Biomarkers ; Inflammation Mediators
Keywords	covid19
Language	English
Publishing date	2020-04-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2020.03.021
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Article ; Online: Loss of regulatory capacity in Treg cells following rhinovirus infection.

The Journal of allergy and clinical immunology

2021 Volume 148, Issue 4, Page(s) 1016–1029.e16

Abstract: Background: Respiratory infections with rhinoviruses (RV) are strongly associated with development and exacerbations of asthma, and they pose an additional health risk for subjects with allergy.: Objective: How RV infections and chronic allergic ... ...

Abstract	Background: Respiratory infections with rhinoviruses (RV) are strongly associated with development and exacerbations of asthma, and they pose an additional health risk for subjects with allergy. Objective: How RV infections and chronic allergic diseases are linked and what role RV plays in the breaking of tolerance in regulatory T (Treg) cells is unknown. Therefore, this study aims to investigate the effects of RV on Treg cells. Methods: Treg cells were isolated from subjects with asthma and controls after experimental infection with the RV-A16 (RV16) and analyzed with next-generation sequencing. Additionally, suppression assays, quantitative PCR assays, and protein quantifications were performed with Treg cells after in vitro RV16 infection. Results: RV16 induced a strong antiviral response in Treg cells from subjects with asthma and controls, including the upregulation of IFI44L, MX1, ISG15, IRF7, and STAT1. In subjects with asthma, the inflammatory response was exaggerated and showed a dysregulated immune response compared with that in the controls. Furthermore, subjects with asthma failed to upregulate several immunosuppressive molecules such as CTLA4 and CD69, and they upregulated the inflammasome-related genes PYCARD and AIM2. Additionally, RV16 reduced the suppressive capacity of Treg cells from healthy subjects and subjects with asthma in vitro and increased T Conclusions: Treg cells from healthy subjects and subjects with asthma displayed an antiviral response after RV infection and showed reduced suppressive capacity. These data suggest that Treg cell function might be altered or impaired during RV infections, which might play an important role in the association between RV and the development of asthma and asthma exacerbations.
MeSH term(s)	Adolescent ; Adult ; Asthma/immunology ; Cytokines/immunology ; Female ; Humans ; Male ; Picornaviridae Infections/immunology ; Rhinovirus/genetics ; T-Lymphocytes, Regulatory/immunology ; Young Adult
Chemical Substances	Cytokines
Language	English
Publishing date	2021-06-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2021.05.045
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Article ; Online: Chapter 37 Infections

Message, Simon D. / Johnston, Sebastian L.

Asthma and COPD

Abstract: Publisher Summary This chapter reviews the epidemiological evidence implicating infectious pathogens as triggers and will discuss the mechanisms of interaction between the host–pathogen response and preexisting airway pathology that result in an ... ...

Abstract	Publisher Summary This chapter reviews the epidemiological evidence implicating infectious pathogens as triggers and will discuss the mechanisms of interaction between the host–pathogen response and preexisting airway pathology that result in an exacerbation. Asthma is a multifaceted syndrome involving atopy, bronchial hyperreactivity, and IgE and non-IgE-mediated acute and chronic immune responses. The asthmatic airway is characterized by an infiltrate of eosinophils and of T-lymphocytes expressing the type 2 cytokines IL-4, IL-5, and IL-13. Trigger factors associated with acute exacerbations of asthma include exposure to environmental allergens, especially animals, molds, pollens and mites, cold, exercise, and drugs. The frequency of exacerbations is a major factor in the quality of life of patients with COPD. The typical clinical features of an exacerbation include increased dyspnea, wheezing, cough, sputum production, and worsened gas exchange. Although noninfectious causes of exacerbations such as allergy, air pollution, or inhaled irritants including cigarette smoke may be important, acute airway infections are the major precipitants. The infection and consequent host inflammatory response result in increased airway obstruction. The success of vaccination to prevent respiratory virus infections has been limited by significant variation within the major virus types causing disease. Currently much of the treatment of infective exacerbations of asthma and COPD is symptomatic, consisting of increased bronchodilators, either short-acting β 2—agonists in inhaled or intravenous form or anticholinergics or theophyllines, or supportive in the form of oxygen and in severe cases noninvasive or invasive ventilatory measures.
Keywords	covid19
Publisher	Elsevier; PMC
Document type	Article ; Online
DOI	10.1016/b978-0-12-374001-4.00037-7
Database	COVID19

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Article ; Online: Infections

Message, Simon D. / Johnston, Sebastian L.

Asthma and COPD

Abstract: This chapter reviews the epidemiological evidence implicating infectious pathogens as triggers and will discuss the mechanisms of interaction between the host–pathogen response and preexisting airway pathology that result in an exacerbation. Asthma is a ... ...

Abstract	This chapter reviews the epidemiological evidence implicating infectious pathogens as triggers and will discuss the mechanisms of interaction between the host–pathogen response and preexisting airway pathology that result in an exacerbation. Asthma is a multifaceted syndrome involving atopy, bronchial hyperreactivity, and IgE and non-IgE-mediated acute and chronic immune responses. The asthmatic airway is characterized by an infiltrate of eosinophils and of T-lymphocytes expressing the type 2 cytokines IL-4, IL-5, and IL-13. Trigger factors associated with acute exacerbations of asthma include exposure to environmental allergens, especially animals, molds, pollens and mites, cold, exercise, and drugs. The frequency of exacerbations is a major factor in the quality of life of patients with COPD. The typical clinical features of an exacerbation include increased dyspnea, wheezing, cough, sputum production, and worsened gas exchange. Although noninfectious causes of exacerbations such as allergy, air pollution, or inhaled irritants including cigarette smoke may be important, acute airway infections are the major precipitants. The infection and consequent host inflammatory response result in increased airway obstruction. The success of vaccination to prevent respiratory virus infections has been limited by significant variation within the major virus types causing disease. Currently much of the treatment of infective exacerbations of asthma and COPD is symptomatic, consisting of increased bronchodilators, either short-acting β 2—agonists in inhaled or intravenous form or anticholinergics or theophyllines, or supportive in the form of oxygen and in severe cases noninvasive or invasive ventilatory measures.
Keywords	covid19
Publisher	Elsevier; PMC
Document type	Article ; Online
DOI	10.1016/b978-0-12-374001-4.00037-7
Database	COVID19

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Article: Host defense function of the airway epithelium in health and disease: clinical background.

Message, Simon D / Johnston, Sebastian L

Journal of leukocyte biology

2003 Volume 75, Issue 1, Page(s) 5–17

Abstract: Respiratory infection is extremely common and a major cause of morbidity and mortality worldwide. The airway epithelium has an important role in host defense against infection and this is illustrated in this review by considering infection by respiratory ...

Abstract	Respiratory infection is extremely common and a major cause of morbidity and mortality worldwide. The airway epithelium has an important role in host defense against infection and this is illustrated in this review by considering infection by respiratory viruses. In patients with asthma or chronic obstructive pulmonary disease, respiratory viruses are a common trigger of exacerbations. Rhinoviruses (RV) are the most common virus type detected. Knowledge of the immunopathogenesis of such RV-induced exacerbations remains limited, but information is available from in vitro and from in vivo studies, especially of experimental infection in human volunteers. RV infects and replicates within epithelial cells (EC) of the lower respiratory tract. EC are an important component of the innate-immune response to RV infection. The interaction between virus and the intracellular signaling pathways of the host cell results in activation of potentially antiviral mechanisms, including type 1 interferons and nitric oxide, and in the production of cytokines and chemokines [interleukin (IL)-1 beta, IL-6, IL-8, IL-11, IL-16, tumor necrosis factor alpha, granulocyte macrophage-colony stimulating factor, growth-regulated oncogene-alpha, epithelial neutrophil-activating protein-78, regulated on activation, normal T expressed and secreted, eotaxin 1/2, macrophage-inflammatory protein-1 alpha], which influence the subsequent induced innate- and specific-immune response. Although this is beneficial in facilitating clearance of virus from the respiratory tract, the generation of proinflammatory mediators and the recruitment of inflammatory cells result in a degree of immunopathology and may amplify pre-existing airway inflammation. Further research will be necessary to determine whether modification of EC responses to respiratory virus infection will be of therapeutic benefit.
MeSH term(s)	Adult ; Asthma/physiopathology ; Chemokines/physiology ; Child ; Cytokines/physiology ; Humans ; Infant ; Reference Values ; Respiratory Mucosa/immunology ; Respiratory Mucosa/physiology ; Respiratory Mucosa/physiopathology ; Respiratory Tract Diseases/physiopathology ; Virus Diseases/physiopathology
Chemical Substances	Chemokines ; Cytokines
Keywords	covid19
Language	English
Publishing date	2003-09-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1189/jlb.0703315
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Article: Viruses in asthma.

Message, Simon D / Johnston, Sebastian L

British medical bulletin

2002 Volume 61, Page(s) 29–43

Abstract: Current evidence suggests that the overall load of infectious agents, including respiratory viruses, encountered early in life is an important factor influencing maturation of the immune system from a type 2 bias at birth towards predominantly type 1 ... ...

Abstract	Current evidence suggests that the overall load of infectious agents, including respiratory viruses, encountered early in life is an important factor influencing maturation of the immune system from a type 2 bias at birth towards predominantly type 1 responses, thus avoiding atopic diseases. The 'hygiene hypothesis' proposes that the relatively sterile environment present in industrialised Western countries has contributed to the recent epidemic of asthma and atopy. Whether specific infections are of greater or lesser protective value is an important question if strategies are to be derived to mimic the beneficial effects of childhood infection whilst avoiding morbidity and potential mortality of the natural pathogens. Infection by respiratory viruses is a major trigger of wheezing in infants and of exacerbations of asthma in older children. Viruses are detected in up to 85% of such episodes. Rhinovirus is common in all age groups; respiratory syncytial virus (RSV) is most important in infants and young children. Knowledge of the immunopathogenetic mechanisms of virus infection in the asthmatic airway will lead to the development of new treatments for virus-induced asthma.
MeSH term(s)	Adolescent ; Adult ; Asthma/epidemiology ; Asthma/immunology ; Asthma/virology ; Developed Countries ; Global Health ; Humans ; Hypersensitivity/epidemiology ; Hypersensitivity/immunology ; Hypersensitivity/virology ; Infant ; Infant, Newborn ; Prevalence ; Respiratory Tract Infections/epidemiology ; Respiratory Tract Infections/immunology ; Th1 Cells/immunology ; Th2 Cells/immunology
Keywords	covid19
Language	English
Publishing date	2002-01-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	213294-1
ISSN	1471-8391 ; 0007-1420
ISSN (online)	1471-8391
ISSN	0007-1420
DOI	10.1093/bmb/61.1.29
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Article ; Online: Ethnic Differences in Severe Asthma Clinical Care and Outcomes: An Analysis of United Kingdom Primary and Specialist Care.

Busby, John / Heaney, Liam G / Brown, Thomas / Chaudhuri, Rekha / Dennison, Paddy / Gore, Robin / Jackson, David J / Mansur, Adel H / Menzies-Gow, Andrew / Message, Simon / Niven, Rob / Patel, Mitesh / Price, David / Siddiqui, Salman / Stone, Robert / Pfeffer, Paul E

The journal of allergy and clinical immunology. In practice

2021 Volume 10, Issue 2, Page(s) 495–505.e2

Abstract: Background: Understanding the effects of ethnicity in severe asthma is important for optimal personalized patient care.: Objective: To assess ethnic differences in disease control, exacerbations, biological phenotype, and treatment in severe asthma ... ...

Abstract	Background: Understanding the effects of ethnicity in severe asthma is important for optimal personalized patient care. Objective: To assess ethnic differences in disease control, exacerbations, biological phenotype, and treatment in severe asthma in the United Kingdom. Methods: We compared demographics, type 2 biomarkers, lung function, asthma control, medications, and health care use between White and underrepresented ethnic group patients in the UK Severe Asthma Registry (UKSAR) and Optimum Patient Care Research Database (OPCRD). Results: A total of 3637 patients (665 from the underrepresented ethnic group) were included from UKSAR and 10,549 (577 from the underrepresented ethnic group) from OPCRD. Patients in the underrepresented ethnic group had higher levels of uncontrolled disease when measurements were made using the asthma control questionnaire in UKSAR (odds ratio [OR] = 1.47; 95% confidence interval [CI], 1.12-1.93) and the Royal College of Physicians 3 Questions in OPCRD (OR = 1.82; 95% CI, 1.27-2.60). Although exacerbation rates were similar, patients in the underrepresented ethnic group were more likely to have recently attended the emergency department (OR = 1.55; 95% CI, 1.26-1.92) or to have been hospitalized (OR = 1.31; 95% CI, 1.07-1.59) owing to asthma. Inflammatory biomarkers were consistently higher in the underrepresented ethnic group, including blood eosinophils in OPCRD (ratio = 1.12; 95% CI, 1.05-1.20) and in UKSAR blood eosinophils (ratio = 1.16; 95% CI, 1.06-1.27), FeNO (ratio = 1.14; 95% CI, 1.04-1.26), and IgE (ratio = 1.70; 95% CI, 1.47-1.97). Patients in the underrepresented ethnic group were more likely to be atopic in the UKSAR (OR = 1.32; 95% CI, 1.07-1.63) and OPCRD (OR = 1.67; 95% CI, 1.26-2.21), and less likely to be using maintenance oral corticosteroids at referral (OR = 0.75; 95% CI, 0.61-0.92). Conclusions: Severe asthma patients from underrepresented ethnic groups presented with a higher disease burden and were more likely to attend the emergency department. They had a distinct phenotypic presentation and differences in medicine use, with higher levels of type 2 biomarkers.
MeSH term(s)	Adrenal Cortex Hormones/therapeutic use ; Asthma/drug therapy ; Asthma/therapy ; Biomarkers ; Eosinophils ; Humans ; Registries ; United Kingdom/epidemiology
Chemical Substances	Adrenal Cortex Hormones ; Biomarkers
Language	English
Publishing date	2021-10-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	2843237-X
ISSN	2213-2201 ; 2213-2198
ISSN (online)	2213-2201
ISSN	2213-2198
DOI	10.1016/j.jaip.2021.09.034
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Article ; Online: Infections

Message, Simon D. / Johnston, Sebastian L.

Asthma and COPD

Abstract: Infection, in particular by respiratory viruses, plays an important role in triggering exacerbations and has also been implicated in the etiology of asthma and chronic obstructive pulmonary disease (COPD). This chapter reviews the epidemiological ... ...

Abstract	Infection, in particular by respiratory viruses, plays an important role in triggering exacerbations and has also been implicated in the etiology of asthma and chronic obstructive pulmonary disease (COPD). This chapter reviews the epidemiological evidence that implicates infectious pathogens as triggers. The chapter also discusses the mechanisms of interaction between the host-pathogen response and preexisting airway pathology resulting in an exacerbation. Much of the treatment of infective exacerbations for both asthma and COPD is symptomatic, consisting of bronchodilators or supportive in the form of oxygen, and in severe cases it includes noninvasive or invasive ventilatory measures. The current therapy for virus-induced exacerbations of asthma and COPD relies on increased treatment of preexisting disease. Antibiotics are indicated for bacterial infections. The effective use of antiviral agents, particularly for influenza viruses, requires viral diagnosis, commencement of treatment early in the course of an exacerbation, or the targeting of high-risk groups for prophylaxis. Alternative strategies for drug development involve the identification of key factors common to exacerbations induced by a range of different viruses. Increased knowledge of the host–virus interaction can help in designing treatments that can increase virus clearance and minimize immunopathology.
Keywords	covid19
Publisher	PMC
Document type	Article ; Online
DOI	10.1016/b978-012079028-9/50114-9
Database	COVID19

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