ArticleEBioMedicine2015
IL-22 Defect During Streptococcus pneumoniae Infection Triggers Exacerbation of Chronic Obstructive Pulmonary Disease.
Article in EBioMedicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- The Human Respiratory Microbiome: Current Understandings and Future Directions.American journal of respiratory cell and molecular biology · 2023Pooled it
- Interleukin-23 in lung and airway diseases: from pathogenesis to precision-guided therapeutic targeting.Frontiers in pharmacology · 2026Review
- Interleukin-10 family cytokines: key regulators and novel therapeutic targets for respiratory diseases.Inflammopharmacology · 2025Review
- Baicalin restores innate lymphoid immune imbalance during exacerbation of COPD.Immunologic research · 2025Article
- Natural Killer Cells as a Further Insight into the Course of Chronic Obstructive Pulmonary Disease.Biomedicines · 2024Article
- Abnormal expression of CD96 on natural killer cell in peripheral blood of patients with chronic obstructive pulmonary disease.The clinical respiratory journal · 2022Article
- Pneumococcal Phasevarions Control Multiple Virulence Traits, Including Vaccine Candidate Expression.Microbiology spectrum · 2022Article
- Contribution of Invariant Natural Killer T Cells to the Clearance ofInternational journal of molecular sciences · 2021Article
- IL-17 AggravatesFrontiers in immunology · 2021Article
- NK Cells in the Pathogenesis of Chronic Obstructive Pulmonary Disease.Frontiers in immunology · 2021Review
- Article
- Boosting the IL-22 response using flagellin prevents bacterial infection in cigarette smoke-exposed mice.Clinical and experimental immunology · 2020Article
- Article
- Th1/Th17 Cytokine Profiles are Associated with Disease Severity and Exacerbation Frequency in COPD Patients.International journal of chronic obstructive pulmonary disease · 2020Article
- Nicotine Impairs the Response of Lung Epithelial Cells to IL-22.Mediators of inflammation · 2020Article
- Electronic cigarette vapour increases virulence and inflammatory potential of respiratory pathogens.Respiratory research · 2019Article
- IL-22 and its receptors are increased in human and experimental COPD and contribute to pathogenesis.The European respiratory journal · 2019Article
- The Influence of Innate Lymphoid Cells and Unconventional T Cells in Chronic Inflammatory Lung Disease.Frontiers in immunology · 2019Review
- Production of Interleukin-20 cytokines limits bacterial clearance and lung inflammation during infection by Streptococcus pneumoniae.EBioMedicine · 2018Article
- IL22 PromotesCancer immunology research · 2018Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Progression of chronic obstructive pulmonary disease (COPD) is linked to episodes of exacerbations caused by bacterial infections due to Streptococcus pneumoniae. Our objective was to identify during COPD, factors of susceptibility to bacterial infections among cytokine network and their role in COPD exacerbations. S. pneumoniae was used to sub-lethally challenge mice chronically exposed to air or cigarette smoke (CS) and to stimulate peripheral blood mononuclear cells (PBMC) from non-smokers, smokers and COPD patients. The immune response and the cytokine production were evaluated. Delayed clearance of the bacteria and stronger lung inflammation observed in infected CS-exposed mice were associated with an altered production of IL-17 and IL-22 by innate immune cells. This defect was related to a reduced production of IL-1β and IL-23 by antigen presenting cells. Importantly, supplementation with recombinant IL-22 restored bacterial clearance in CS-exposed mice and limited lung alteration. In contrast with non-smokers, blood NK and NKT cells from COPD patients failed to increase IL-17 and IL-22 levels in response to S. pneumoniae, in association with a defect in IL-1β and IL-23 secretion. This study identified IL-17 and IL-22 as susceptibility factors in COPD exacerbation. Therefore targeting such cytokines could represent a potent strategy to control COPD exacerbation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.