Imperial College London

ProfessorSebastianJohnston

Faculty of MedicineNational Heart & Lung Institute

Asthma UK Clinical Chair
 
 
 
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Contact

 

+44 (0)20 7594 3764s.johnston

 
 
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Assistant

 

Mr Christophe Tytgat +44 (0)20 7594 3849

 
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Location

 

343Norfolk PlaceSt Mary's Campus

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Summary

 

Publications

Publication Type
Year
to

546 results found

Teo SM, Mok D, Pham K, Kusel M, Serralha M, Troy N, Holt BJ, Hales BJ, Walker ML, Hollams E, Bochkov YA, Grindle K, Johnston SL, Gern JE, Sly PD, Holt PG, Holt KE, Inouye Met al., 2015, The Infant Nasopharyngeal Microbiome Impacts Severity of Lower Respiratory Infection and Risk of Asthma Development, Cell Host & Microbe, Vol: 17, Pages: 704-715, ISSN: 1934-6069

The nasopharynx (NP) is a reservoir for microbes associated with acute respiratory infections (ARIs). Lung inflammation resulting from ARIs during infancy is linked to asthma development. We examined the NP microbiome during the critical first year of life in a prospective cohort of 234 children, capturing both the viral and bacterial communities and documenting all incidents of ARIs. Most infants were initially colonized with Staphylococcus or Corynebacterium before stable colonization with Alloiococcus or Moraxella. Transient incursions of Streptococcus, Moraxella, or Haemophilus marked virus-associated ARIs. Our data identify the NP microbiome as a determinant for infection spread to the lower airways, severity of accompanying inflammatory symptoms, and risk for future asthma development. Early asymptomatic colonization with Streptococcus was a strong asthma predictor, and antibiotic usage disrupted asymptomatic colonization patterns. In the absence of effective anti-viral therapies, targeting pathogenic bacteria within the NP microbiome could represent a prophylactic approach to asthma.

Journal article

Contoli M, Ito K, Padovani A, Poletti D, Marku B, Edwards MR, Stanciu LA, Gnesini G, Pastore A, Spanevello A, Morelli P, Johnston SL, Caramori G, Papi Aet al., 2015, Th2 cytokines impair innate immune responses to rhinovirus in respiratory epithelial cells, Allergy, Vol: 70, Pages: 910-920, ISSN: 0105-4538

BackgroundAsthma and other Th2 inflammatory conditions have been associated with increased susceptibility to viral infections. The mechanisms by which Th2 cytokines can influence immune responses to infections are largely unknown.MethodsWe measured the effects of Th2 cytokines (IL-4 and IL-13) on bronchial epithelial cell innate immune antiviral responses by assessing interferon (IFN-β and IFN-λ1) induction following rhinovirus (RV)-16 infection. We also investigated the modulatory effects of Th2 cytokines on Toll-like receptor 3 (TLR3), interferon-responsive factor 3 (IRF3) and nuclear factor (NF)-kB, that is key molecules and transcription factors involved in the rhinovirus-induced interferon production and inflammatory cascade. Pharmacological and redox modulation of these pathways was also assessed.ResultsTh2 cytokines impaired RV-16-induced interferon production, increased rhinovirus replication and impaired TLR3 expression in bronchial epithelial cells. These results were replicated in vivo: we found increased IL-4 mRNA levels in nasal epithelial cells from nasal brushing of atopic rhinitis patients and a parallel reduction in TLR3 expression and increased RV-16 replication compared to nonatopic subjects. Mechanistically, Th2 cytokines impaired RV-16-induced activation of IRF3, but had no effects on RV-16-induced NF-kB activation in bronchial epithelial cell cultures. N-acetylcysteine and phosphoinositide 3-kinase (PI3K) inhibitor restored the inhibitory effects of Th2 cytokines over RV-16-induced activation of IRF3.ConclusionsIL-4 and IL-13, through inhibition of TLR3 expression and signalling (IRF3), impair immune response to RV-16 infection. These data suggest that Th2 conditions increase susceptibility to infections and identify pharmacological approaches with potential to restore impaired immune response in these conditions.

Journal article

Holt PG, Teo SM, Mok D, Pham K, Kusel M, Serralha M, Troy N, Holt BJ, Hales B, Walker ML, Hollams EM, Bochkov YH, Grindle K, Johnston SL, Gern JE, Sly PD, Holt KE, Inouye Met al., 2015, The infant nasopharyngeal microbiome impacts severity of lower respiratory infection and risk of asthma development, Cell Host and Microbe, Vol: 17, Pages: 704-715, ISSN: 1931-3128

The nasopharynx (NP) is a reservoir for microbes associated with acute respiratory infections (ARIs). Lung inflammation resulting from ARIs during infancy is linked to asthma development. We examined the NP microbiome during the critical first year of life in a prospective cohort of 234 children, capturing both the viral and bacterial communities and documenting all incidents of ARIs. Most infants were initially colonized with Staphylococcus or Corynebacterium before stable colonization with Alloiococcus or Moraxella. Transient incursions of Streptococcus, Moraxella, or Haemophilus marked virus-associated ARIs. Our data identify the NP microbiome as a determinant for infection spread to the lower airways, severity of accompanying inflammatory symptoms, and risk for future asthma development. Early asymptomatic colonization with Streptococcus was a strong asthma predictor, and antibiotic usage disrupted asymptomatic colonization patterns. In the absence of effective anti-viral therapies, targeting pathogenic bacteria within the NP microbiome could represent a prophylactic approach to asthma.

Journal article

Bonnelykke K, Vissing NH, Sevelsted A, Johnston SL, Bisgaard Het al., 2015, Association between respiratory infections in early life and later asthma is independent of virus type, ALERGOLOGIA POLSKA-POLISH JOURNAL OF ALLERGOLOGY, Vol: 2, Pages: T25-T35, ISSN: 2353-3854

Journal article

Glanville N, Johnston SL, 2015, Challenges in developing a cross-serotype rhinovirus vaccine, Current Opinion in Virology, Vol: 11, Pages: 83-88, ISSN: 1879-6257

A great burden of disease is attributable to human rhinovirus (HRV) infections which are the major cause of the common cold, exacerbations of both asthma and chronic obstructive pulmonary disease (COPD), and are associated with asthma development. Despite this there is currently no vaccine for HRV. The first vaccine studies showed some promise in terms of serotype-specific protection against cold symptoms, but antigenic heterogeneity amongst the >150 HRVs has been regarded as a major barrier to effective vaccine development and has resulted in little progress over 50 years. Here we review those vaccine studies conducted to date, discuss the difficulties posed by antigenic heterogeneity and describe some recent advances in generating cross-reactive antibodies and T cell responses using peptide immunogens.

Journal article

Schapowal A, Klein P, Johnston SL, 2015, Echinacea Reduces the Risk of Recurrent Respiratory Tract Infections and Complications: A Meta-Analysis of Randomized Controlled Trials, ADVANCES IN THERAPY, Vol: 32, Pages: 187-200, ISSN: 0741-238X

Journal article

Singanayagam A, Glanville N, Bartlett N, Johnston Set al., 2015, Effect of fluticasone propionate on virus-induced airways inflammation and anti-viral immune responses in mice, Spring Meeting on Clinician Scientists in Training, Publisher: ELSEVIER SCIENCE INC, Pages: 88-88, ISSN: 0140-6736

Conference paper

Drysdale SB, Alcazar-Paris M, Wilson T, Smith M, Zuckerman M, Peacock JL, Johnston SL, Greenough Aet al., 2015, Viral lower respiratory tract infections and preterm infants' healthcare utilisation, EUROPEAN JOURNAL OF PEDIATRICS, Vol: 174, Pages: 209-215, ISSN: 0340-6199

Journal article

Schogler A, Kopf BS, Edwards MR, Johnston SL, Casaultal C, Kieninger E, Jung A, Moeller A, Geiser T, Regamey N, Alves MPet al., 2015, Novel antiviral properties of azithromycin in cystic fibrosis airway epithelial cells, EUROPEAN RESPIRATORY JOURNAL, Vol: 45, Pages: 428-439, ISSN: 0903-1936

Journal article

Cameron A, Dhariwal J, Johnston SL, Walton RPet al., 2015, Rhinovirus Modulation of Dendritic Cell Phenotype and Function, Annual Meeting of the American-Academy-of-Allergy-Asthma-and-Immunology (AAAAI), Publisher: MOSBY-ELSEVIER, Pages: AB63-AB63, ISSN: 0091-6749

Conference paper

Lan F, Zhang N, Holtappels G, De Ruyck N, Papadopoulos NG, Johnston SL, Bachert Cet al., 2015, Staphyloccoccus Aureus Induces a Th2 Response Via TSLP and IL-33 Release in Human Airway Mucosa, Annual Meeting of the American-Academy-of-Allergy-Asthma-and-Immunology (AAAAI), Publisher: MOSBY-ELSEVIER, Pages: AB81-AB81, ISSN: 0091-6749

Conference paper

Hilzendeger C, Da Silva J, Henket M, Moermans C, Corhay J-L, Edwards M, Johnston SL, Louis Ret al., 2015, Expression Of Interferons And Interferon-Stimulated Genes In Peripheral-Blood Neutrophils From COPD Patients, International Conference of the American-Thoracic-Society (ATS), Publisher: AMER THORACIC SOC, ISSN: 1073-449X

Conference paper

Almond MH, Bakhsoliani E, Edwards MR, Barclay WS, Johnston SLet al., 2015, Obesity Is Associated With Decreased Expression Of Suppressor Of Cytokine Signalling 3 In Human Alveolar Macrophages, International Conference of the American-Thoracic-Society (ATS), Publisher: AMER THORACIC SOC, ISSN: 1073-449X

Conference paper

Toussaint M, Footitt J, Trujillo-Torralbo M-B, Kebadze T, Aniscenko J, Del Rosario A, Adcock IM, Johnston SL, Mallia Pet al., 2015, Airway Dna Levels In Virus-Induced COPD Exacerbations, International Conference of the American-Thoracic-Society (ATS), Publisher: AMER THORACIC SOC, ISSN: 1073-449X

Conference paper

Singanayagam A, Johnston SL, Mallia P, 2015, Inhaled Glucocorticoids and COPD Exacerbations, New England Journal of Medicine, Vol: 372, Pages: 92-93, ISSN: 1533-4406

Journal article

Calderazzo M, Trujillo-Torralbo M, Finney LJ, Kebadze T, Johnston SL, Mallia Pet al., 2015, Relationship Between Viral Colds And COPD Exacerbations, International Conference of the American-Thoracic-Society (ATS), Publisher: AMER THORACIC SOC, ISSN: 1073-449X

Conference paper

Bartlett NW, Singanayagam A, Johnston SL, 2015, Mouse models of rhinovirus infection and airways disease., Methods Mol Biol, Vol: 1221, Pages: 181-188

Mouse models are invaluable tools for gaining insight into host immunity during virus infection. Until recently, no practical mouse model for rhinovirus infection was available. Development of infection models was complicated by the existence of distinct groups of viruses that utilize different host cell surface proteins for binding and entry. Here, we describe mouse infection models, including virus purification and measurement of host immune responses, for representative viruses from two of these groups: (1) infection of unmodified Balb/c mice with minor group rhinovirus serotype 1B (RV-1B) and (2) infection of transgenic Balb/c mice with major group rhinovirus serotype 16 (RV-16).

Journal article

Teo SM, Mok D, Pham K, Kusel M, Serralha M, Troy N, Holt BJ, Hales BJ, Walker ML, Hollams E, Bochkov YH, Grindle K, Johnston SL, Gern JE, Sly PD, Holt PG, Holt KE, Inouye Met al., 2014, The infant airway microbiome in health and disease impacts later asthma development

<jats:p>The nasopharynx (NP) is a reservoir for microbes associated with acute respiratory illnesses (ARI). The development of asthma is initiated during infancy, driven by airway inflammation associated with infections. Here, we report viral and bacterial community profiling of NP aspirates across a birth cohort, capturing all lower respiratory illnesses during their first year. Most infants were initially colonized with Staphylococcus or Corynebacterium before stable colonization with Alloiococcus or Moraxella, with transient incursions of Streptococcus, Moraxella or Haemophilus marking virus-associated ARIs. Our data identify the NP microbiome as a determinant for infection spread to the lower airways, severity of accompanying inflammatory symptoms, and risk for future asthma development. Early asymptomatic colonization with Streptococcus was a strong asthma predictor, and antibiotic usage disrupted asymptomatic colonization patterns.</jats:p>

Journal article

Johnston SL, Zdrenghea MT, Makrinioti H, Muresan A, Stanciu LAet al., 2014, The role of macrophage IL-10/innate IFN interplay during virus-induced asthma, Reviews in Medical Virology, Vol: 25, Pages: 33-49, ISSN: 1099-1654

Activation through different signaling pathways results in two functionally different types of macrophages, the pro-inflammatory (M1) and the anti-inflammatory (M2). The polarization of macrophages toward the pro-inflammatory M1 phenotype is considered to be critical for efficient antiviral immune responses in the lung.Among the various cell types that are present in the asthmatic airways, macrophages have emerged as significant participants in disease pathogenesis, because of their activation during both the inflammatory and resolution phases, with an impact on disease progression. Polarized M1 and M2 macrophages are able to reversibly undergo functional redifferentiation into anti-inflammatory or pro-inflammatory macrophages, respectively, and therefore, macrophages mediate both processes.Recent studies have indicated a predominance of M2 macrophages in asthmatic airways. During a virus infection, it is likely that M2 macrophages would secrete higher amounts of the suppressor cytokine IL-10, and less innate IFNs. However, the interactions between IL-10 and innate IFNs during virus-induced exacerbations of asthma have not been well studied.The possible role of IL-10 as a therapy in allergic asthma has already been suggested, but the divergent roles of this suppressor molecule in the antiviral immune response raise concerns. This review attempts to shed light on macrophage IL-10–IFNs interactions and discusses the role of IL-10 in virus-induced asthma exacerbations. Whereas IL-10 is important in terminating pro-inflammatory and antiviral immune responses, the presence of this immune regulatory cytokine at the beginning of virus infection could impair the response to viruses and play a role in virus-induced asthma exacerbations.

Journal article

Niespodziana K, Cabauatan CR, Jackson DJ, Gallerano D, Trujillo-Torralbo B, Del Rosario A, Mallia P, Valenta R, Johnston SLet al., 2014, Rhinovirus-induced VP1-specific Antibodies are Group-specific and Associated With Severity of Respiratory Symptoms., EBioMedicine, Vol: 2, Pages: 64-70, ISSN: 2352-3964

BACKGROUND: Rhinoviruses (RVs) are a major cause of common colds and induce exacerbations of asthma and chronic inflammatory lung diseases. METHODS: We expressed and purified recombinant RV coat proteins VP1-4, non-structural proteins as well as N-terminal fragments of VP1 from four RV strains (RV14, 16, 89, C) covering the three known RV groups (RV-A, RV-B and RV-C) and measured specific IgG-subclass-, IgA- and IgM-responses by ELISA in subjects with different severities of asthma or without asthma before and after experimental infection with RV16. FINDINGS: Before infection subjects showed IgG1 > IgA > IgM > IgG3 cross-reactivity with N-terminal fragments from the representative VP1 proteins of the three RV groups. Antibody levels were higher in the asthmatic group as compared to the non-asthmatic subjects. Six weeks after infection with RV16, IgG1 antibodies showed a group-specific increase towards the N-terminal VP1 fragment, but not towards other capsid and non-structural proteins, which was highest in subjects with severe upper and lower respiratory symptoms. INTERPRETATION: Our results demonstrate that increases of antibodies towards the VP1 N-terminus are group-specific and associated with severity of respiratory symptoms and suggest that it may be possible to develop serological tests for identifying causative RV groups.

Journal article

Finney L, Berry M, Singanayagam A, Elkin SL, Johnston SL, Mallia Pet al., 2014, Inhaled corticosteroids and pneumonia in chronic obstructive pulmonary disease, LANCET RESPIRATORY MEDICINE, Vol: 2, Pages: 919-932, ISSN: 2213-2600

Journal article

Drysdale SB, Lo J, Prendergast M, Alcazar M, Wilson T, Zuckerman M, Smith M, Broughton S, Rafferty GF, Peacock JL, Johnston SL, Greenough Aet al., 2014, Lung function of preterm infants before and after viral infections, EUROPEAN JOURNAL OF PEDIATRICS, Vol: 173, Pages: 1497-1504, ISSN: 0340-6199

Journal article

Jackson DJ, Makrinioti H, Rana BMJ, Shamji BWH, Trujillo-Torralbo M-B, Footitt J, Del-Rosario J, Telcian AG, Nikonova A, Zhu J, Aniscenko J, Gogsadze L, Bakhsoliani E, Traub S, Dhariwal J, Porter J, Hunt D, Hunt T, Hunt T, Stanciu LA, Khaitov M, Bartlett NW, Edwards MR, Kon OM, Mallia P, Papadopoulos NG, Akdis CA, Westwick J, Edwards MJ, Cousins DJ, Walton RP, Johnston SLet al., 2014, IL-33-Dependent Type 2 Inflammation during Rhinovirus-induced Asthma Exacerbations In Vivo, American Journal of Respiratory and Critical Care Medicine, Vol: 190, Pages: 1373-1382, ISSN: 1535-4970

Rationale: Rhinoviruses are the major cause of asthmaexacerbations; however, its underlying mechanisms are poorlyunderstood. We hypothesized that the epithelial cell–derivedcytokine IL-33 plays a central role in exacerbation pathogenesisthrough augmentation of type 2 inflammation.Objectives: To assess whether rhinovirus induces a type 2inflammatory response in asthma in vivo and to define a role for IL-33in this pathway.Methods: We used a human experimental model of rhinovirusinfection and novel airway sampling techniques to measure IL-4, IL-5,IL-13, and IL-33 levels in the asthmatic and healthy airways duringa rhinovirus infection. Additionally, we cultured human T cells and type2 innate lymphoid cells (ILC2s) with the supernatants of rhinovirusinfectedbronchial epithelial cells (BECs) to assess type 2 cytokineproduction in the presence or absence of IL-33 receptor blockade.Measurements and Main Results: IL-4, IL-5, IL-13, and IL-33 areall induced by rhinovirus in the asthmatic airway in vivo and relate toexacerbation severity. Further, induction of IL-33 correlates withviral load and IL-5 and IL-13 levels. Rhinovirus infection of humanprimary BECs induced IL-33, and culture of human T cells and ILC2swith supernatants of rhinovirus-infected BECs strongly inducedtype 2 cytokines. This induction was entirely dependent on IL-33.Conclusions: IL-33 and type 2 cytokines are induced duringa rhinovirus-induced asthma exacerbation in vivo. Virus-inducedIL-33 and IL-33–responsive T cells and ILC2s are key mechanisticlinks between viral infection and exacerbation of asthma. IL-33inhibition is a novel therapeutic approach for asthma exacerbations

Journal article

Molyneaux PL, Cox MJ, Willis-Owen SAG, Mallia P, Russell KE, Russel A-M, Murphy E, Johnston SL, Schwarte DA, Wells AU, Cookson WOC, Maher TM, Moffatt MFet al., 2014, The Role of Bacteria in the Pathogenesis and Progression of Idiopathic Pulmonary Fibrosis, American Journal of Respiratory and Critical Care Medicine, Vol: 190, Pages: 906-913, ISSN: 1535-4970

Rationale:Idiopathic pulmonaryfibrosis (IPF)isa progressivelung diseaseof unknown cause that leads to respiratory failure and death within 5 yearsof diagnosis. Overt respiratory infection and immunosuppression carrya high morbidity and mortality, and polymorphisms in genes related toepithelial integrity and host defense predispose to IPF.Objectives: To investigate the role of bacteria in the pathogenesisand progression of IPF.Methods: We prospectively enrolled patients diagnosed with IPFaccording to international criteria together with healthy smokers,nonsmokers, and subjectswithmoderate chronic obstructive pulmonarydisease as control subjects. Subjects underwent bronchoalveolarlavage (BAL), from which genomic DNA was isolated. The V3–V5region of the bacterial 16S rRNA gene was amplified, allowingquantification of bacterial load and identification of communities by 16SrRNA quantitative polymerase chain reaction and pyrosequencing. Measurements and Main Results: Sixty-five patients with IPFhad double the burden of bacteria in BAL fluid compared with 44 controlsubjects. Baseline bacterial burden predicted the rate of decline in lungvolume and risk of death and associated independently with thers35705950 polymorphism of the MUC5B mucin gene, a proven hostsusceptibilityfactorfor IPF. Sequencing yielded912,883 high-quality readsfrom all subjects.WeidentifiedHaemophilus, Streptococcus,Neisseria, andVeillonella spp. to be more abundant in cases than control subjects.Regression analyses indicated that these specific operational taxonomicunits as well as bacterial burden associated independently with IPF.Conclusions: IPF is characterized by an increased bacterial burdenin BAL that predicts decline in lung function and death. Trials ofantimicrobial therapy are needed to determine if microbial burdenis pathogenic in the disease.

Journal article

Finney LJ, Ritchie A, Pollard E, Johnston SL, Mallia Pet al., 2014, Lower airway colonization and inflammatory response in COPD: a focus on Haemophilus influenzae, International Journal of Chronic Obstructive Pulmonary Disease, Vol: 9, Pages: 1119-1132, ISSN: 1176-9106

Bacterial infection of the lower respiratory tract in chronic obstructive pulmonary disease (COPD) patients is common both in stable patients and during acute exacerbations. The most frequent bacteria detected in COPD patients is Haemophilus influenzae, and it appears this organism is uniquely adapted to exploit immune deficiencies associated with COPD and to establish persistent infection in the lower respiratory tract. The presence of bacteria in the lower respiratory tract in stable COPD is termed colonization; however, there is increasing evidence that this is not an innocuous phenomenon but is associated with airway inflammation, increased symptoms, and increased risk for exacerbations. In this review, we discuss host immunity that offers protection against H. influenzae and how disturbance of these mechanisms, combined with pathogen mechanisms of immune evasion, promote persistence of H. influenzae in the lower airways in COPD. In addition, we examine the role of H. influenzae in COPD exacerbations, as well as interactions between H. influenzae and respiratory virus infections, and review the role of treatments and their effect on COPD outcomes. This review focuses predominantly on data derived from human studies but will refer to animal studies where they contribute to understanding the disease in humans.

Journal article

Beale J, Jayaraman A, Jackson DJ, Macintyre JDR, Edwards MR, Walton RP, Zhu J, Ching YM, Shamji B, Edwards M, Westwick J, Cousins DJ, Hwang YY, McKenzie A, Johnston SL, Bartlett NWet al., 2014, Rhinovirus-induced IL-25 in asthma exacerbation drives type 2 immunity and allergic pulmonary inflammation, SCIENCE TRANSLATIONAL MEDICINE, Vol: 6, ISSN: 1946-6234

Journal article

Tsoumakidou M, Tousa S, Semitekolou M, Panagiotou P, Panagiotou A, Morianos I, Litsiou E, Trochoutsou AI, Konstantinou M, Potaris K, Footitt J, Mallia P, Zakynthinos S, Johnston SL, Xanthou Get al., 2014, Tolerogenic signaling by pulmonary CD1c(+) dendritic cells induces regulatory T cells in patients with chronic obstructive pulmonary disease by IL-27/IL-10/inducible costimulator ligand, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, Vol: 134, Pages: 944-U282, ISSN: 0091-6749

Journal article

Mousnier A, Swieboda D, Pinto A, Guedan A, Rogers AV, Walton R, Johnston SL, Solari Ret al., 2014, Human Rhinovirus 16 Causes Golgi Apparatus Fragmentation without Blocking Protein Secretion, JOURNAL OF VIROLOGY, Vol: 88, Pages: 11671-11685, ISSN: 0022-538X

Journal article

Nikonova A, Jackson D, Traub S, Johnston SL, Khaitov M, Stanciu LAet al., 2014, Changes in peripheral blood monocytes, B-cells, myeloid and plasmacytoid dendritic cells in asthma patients during rhinovirus-induced exacerbation, European-Academy-of-Allergy-and-Clinical-Immunology Congress, Publisher: WILEY-BLACKWELL, Pages: 147-147, ISSN: 0105-4538

Conference paper

Wolsk HM, Folsgaard N, Birch S, Brix S, Hansel TT, Johnston SL, Kebadze T, Chawes BL, Bonnelykke K, Bisgaard Het al., 2014, The presence of viruses alters the immune signature in the airway of asymptomatic neonates, European-Academy-of-Allergy-and-Clinical-Immunology Congress, Publisher: WILEY-BLACKWELL, Pages: 192-193, ISSN: 0105-4538

Conference paper

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