ArticleInternational journal of chronic obstructive pulmonary disease2016
An antagonist of the platelet-activating factor receptor inhibits adherence of both nontypeable Haemophilus influenzae and Streptococcus pneumoniae to cultured human bronchial epithelial cells exposed to cigarette smoke.
Article in International journal of chronic obstructive pulmonary disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
- Post-influenza bacterial infection: mechanisms of pathogenesis and advances in therapeutic strategies.Frontiers in microbiology · 2025Review
- Associations between Wastewater Microbiome and Population Smoking Rate Identified Using Wastewater-Based Epidemiology.Environment & health (Washington, D.C.) · 2023Article
- Non-typeableEuropean respiratory review : an official journal of the European Respiratory Society · 2022Review
- Underground railway particulate matter and susceptibility to pneumococcal infection.EBioMedicine · 2022Article
- Fully integrating pathophysiological insights in COPD: an updated working disease model to broaden therapeutic vision.European respiratory review : an official journal of the European Respiratory Society · 2021Review
- Draft genome sequence of a nontypeable Haemophilus influenzae strain used in the study of human respiratory infection.BMC research notes · 2021Article
- Honeysuckle (Frontiers in pharmacology · 2021Article
- Influence of Hypoxia on the Epithelial-Pathogen Interactions in the Lung: Implications for Respiratory Disease.Frontiers in immunology · 2021Review
- An in vivo atlas of host-pathogen transcriptomes duringProceedings of the National Academy of Sciences of the United States of America · 2020Article
- The role of NTHi colonization and infection in the pathogenesis of neutrophilic asthma.Respiratory research · 2020Review
- A1 adenosine receptor signaling reduces Streptococcus pneumoniae adherence to pulmonary epithelial cells by targeting expression of platelet-activating factor receptor.Cellular microbiology · 2020Article
- Repeated Exposure to Streptococcus pneumoniae Exacerbates Chronic Obstructive Pulmonary Disease.The American journal of pathology · 2019Article
- Heparin-binding epidermal growth factor (HB-EGF) drives EMT in patients with COPD: implications for disease pathogenesis and novel therapies.Laboratory investigation; a journal of technical methods and pathology · 2019Review
- The role of environmental exposure to non-cigarette smoke in lung disease.Clinical and translational medicine · 2018Review
- E-cigarette vapour enhances pneumococcal adherence to airway epithelial cells.The European respiratory journal · 2018Article
- A cost-effective technique for generating preservable biomass smoke extract and measuring its effect on cell receptor expression in human bronchial epithelial cells.Biology methods & protocols · 2018Article
- Role of Inflammatory Risk Factors in the Pathogenesis ofFrontiers in immunology · 2018Review
- Revisiting cefditoren for the treatment of community-acquired infections caused by human-adapted respiratory pathogens in adults.Multidisciplinary respiratory medicine · 2018Review
- Cigarette smoke promotes COPD by activating platelet-activating factor receptor and inducing neutrophil autophagic death in mice.Oncotarget · 2017Article
- The main rhinovirus respiratory tract adhesion site (ICAM-1) is upregulated in smokers and patients with chronic airflow limitation (CAL).Respiratory research · 2017Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCOPD is emerging as the third largest cause of human mortality worldwide after heart disease and stroke. Tobacco smoking, the primary risk factor for the development of COPD, induces increased expression of platelet-activating factor receptor (PAFr) in the lung epithelium. Nontypeable Haemophilus influenzae (NTHi) and Streptococcus pneumoniae adhere to PAFr on the luminal surface of human respiratory tract epithelial cells.
objectiveTo investigate PAFr as a potential drug target for the prevention of infections caused by the main bacterial drivers of acute exacerbations in COPD patients, NTHi and S. pneumoniae.
methodsHuman bronchial epithelial BEAS-2B cells were exposed to cigarette smoke extract (CSE). PAFr expression levels were determined using immunocytochemistry and quantitative polymerase chain reaction. The epithelial cells were challenged with either NTHi or S. pneumoniae labeled with fluorescein isothiocyanate, and bacterial adhesion was measured using immunofluorescence. The effect of a well-evaluated antagonist of PAFr, WEB-2086, on binding of the bacterial pathogens to BEAS-2B cells was then assessed. In silico studies of the tertiary structure of PAFr and the binding pocket for PAF and its antagonist WEB-2086 were undertaken.
resultsPAFr expression by bronchial epithelial cells was upregulated by CSE, and significantly associated with increased bacterial adhesion. WEB-2086 reduced the epithelial adhesion by both NTHi and S. pneumoniae to levels observed for non-CSE-exposed cells. Furthermore, it was nontoxic toward the bronchial epithelial cells. In silico analyses identified a binding pocket for PAF/WEB-2086 in the predicted PAFr structure.
conclusionWEB-2086 represents an innovative class of candidate drugs for inhibiting PAFr-dependent lung infections caused by the main bacterial drivers of smoking-related COPD.
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