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Your search keyword '"Suado M, Abdillahi"' showing total 3 results
Start Over Author "Suado M, Abdillahi" Topic haemophilus influenzae
3 results on '"Suado M, Abdillahi"'

1. Corrigendum: The pulmonary extracellular matrix is a bactericidal barrier against Haemophilus influenzae in chronic obstructive pulmonary disease (COPD): implications for an in vivo innate host defense function of collagen VI

Author

Suado M. Abdillahi, Ramesh Tati, Sara L. Nordin, Maria Baumgarten, Oskar Hallgren, Leif Bjermer, Jonas Erjefält, Gunilla Westergren-Thorsson, Birendra Singh, Kristian Riesbeck, and Matthias Mörgelin

Subjects
antimicrobial activity, bronchopulmonary infection, collagen VI, COPD, extracellular matrix, Haemophilus influenzae, Immunologic diseases. Allergy, RC581-607
Published
2023
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2. The Pulmonary Extracellular Matrix Is a Bactericidal Barrier Against Haemophilus influenzae in Chronic Obstructive Pulmonary Disease (COPD): Implications for an in vivo Innate Host Defense Function of Collagen VI

Author

Suado M. Abdillahi, Ramesh Tati, Sara L. Nordin, Maria Baumgarten, Oskar Hallgren, Leif Bjermer, Jonas Erjefält, Gunilla Westergren-Thorsson, Birendra Singh, Kristian Riesbeck, and Matthias Mörgelin

Subjects
antimicrobial activity, bronchopulmonary infection, collagen VI, COPD, extracellular matrix, Haemophilus influenzae, Immunologic diseases. Allergy, RC581-607
Abstract

Non-typeable Haemophilus influenzae (NTHi) is a Gram-negative human commensal commonly residing in the nasopharynx of preschool children. It occasionally causes upper respiratory tract infection such as acute otitis media, but can also spread to the lower respiratory tract causing bronchitis and pneumonia. There is increasing recognition that NTHi has an important role in chronic lower respiratory tract inflammation, particularly in persistent infection in patients suffering from chronic obstructive pulmonary disease (COPD). Here, we set out to assess the innate protective effects of collagen VI, a ubiquitous extracellular matrix component, against NTHi infection in vivo. In vitro, collagen VI rapidly kills bacteria through pore formation and membrane rupture, followed by exudation of intracellular content. This effect is mediated by specific binding of the von Willebrand A (VWA) domains of collagen VI to the NTHi surface adhesins protein E (PE) and Haemophilus autotransporter protein (Hap). Similar observations were made in vivo specimens from murine airways and COPD patient biopsies. NTHi bacteria adhered to collagen fibrils in the airway mucosa and were rapidly killed by membrane destabilization. The significance in host-pathogen interplay of one of these molecules, PE, was highlighted by the observation that it confers partial protection from bacterial killing. Bacteria lacking PE were more prone to antimicrobial activity than NTHi expressing PE. Altogether the data shed new light on the carefully orchestrated molecular events of the host-pathogen interplay in COPD and emphasize the importance of the extracellular matrix as a novel branch of innate host defense.

Published
2018
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3. Multi-omics links IL-6 trans-signalling with neutrophil extracellular trap formation andHaemophilusinfection in COPD

Author

Sofia Winslow, Sriram Sridhar, Sofia Lundin, Helena Lindmark, Annika Wellner, Cecilia Wingren, Ratko Djukanovic, Zala Jevnikar, Suado M. Abdillahi, Henric Olsson, Dave Singh, Linda Yrlid, Sarah Diver, Andrew Higham, Lina Odqvist, Christopher E. Brightling, Elisabeth Ax, Rebecca E. Riise, and Thomas Southworth

Subjects
Pulmonary and Respiratory Medicine, COPD, biology, medicine.diagnostic_test, business.industry, Neutrophil extracellular traps, medicine.disease_cause, medicine.disease, Neutrophilia, respiratory tract diseases, Haemophilus influenzae, Bronchoalveolar lavage, Immunology, medicine, biology.protein, Sputum, medicine.symptom, Interleukin 6, business, Asthma
Abstract

Background:Interleukin (IL)-6 trans-signalling (IL-6TS) is emerging as a pathogenic mechanism in chronic respiratory diseases; however, the drivers of IL-6TS in the airways and the phenotypic characteristic of patients with increased IL-6TS pathway activation remain poorly understood.Objective:Our aim was to identify and characterise COPD patients with increased airway IL-6TS and to elucidate the biological drivers of IL-6TS pathway activation.Methods:We used an IL-6TS-specific sputum biomarker profile (soluble IL-6 receptor (sIL-6R), IL-6, IL-1β, IL-8, macrophage inflammatory protein-1β) to stratify sputum data from patients with COPD (n=74; Biomarkers to Target Antibiotic and Systemic Corticosteroid Therapy in COPD Exacerbation (BEAT-COPD)) by hierarchical clustering. The IL-6TS signature was related to clinical characteristics and sputum microbiome profiles. The induction of neutrophil extracellular trap formation (NETosis) and IL-6TS byHaemophilus influenzaewere studied in human neutrophils.Results:Hierarchical clustering revealed an IL-6TS-high subset (n=24) of COPD patients, who shared phenotypic traits with an IL-6TS-high subset previously identified in asthma. The subset was characterised by increased sputum cell counts (p=0.0001), persistent sputum neutrophilia (p=0.0004), reduced quality of life (Chronic Respiratory Questionnaire total score; p=0.008), and increased levels of pro-inflammatory mediators and matrix metalloproteinases in sputum. IL-6TS-high COPD patients showed an increase in Proteobacteria, withHaemophilusas the dominating genus. NETosis induced byH. influenzaewas identified as a potential mechanism for increased sIL-6R levels. This was supported by a significant positive correlation between sIL-6R and NETosis markers in bronchoalveolar lavage fluid from COPD patients.Conclusion:IL-6TS pathway activation due to chronic colonisation withHaemophilusmay be an important disease driver in a subset of COPD patients.

Published
2021
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