PloS one, 2021-01, Vol.16 (1), p.e0243484-e0243484
2021
Details
- Autor(en) / Beteiligte
- Titel
- IL-17C contributes to NTHi-induced inflammation and lung damage in experimental COPD and is present in sputum during acute exacerbations
- Ist Teil von
- PloS one, 2021-01, Vol.16 (1), p.e0243484-e0243484
- Ort / Verlag
- United States: Public Library of Science
- Erscheinungsjahr
- 2021
- Link zum Volltext
- Quelle
- Free E-Journal (出版社公開部分のみ）
- Beschreibungen/Notizen
- Neutrophilic inflammation results in loss of lung function in chronic obstructive pulmonary disease (COPD). Gram-negative bacteria, such as nontypeable Haemophilus influenzae (NTHi), trigger acute exacerbations of COPD (AECOPD) and contribute to chronic lung inflammation. The pro-inflammatory cytokine interleukin-17C (IL-17C) is expressed by airway epithelial cells and regulates neutrophilic chemotaxis. Here, we explored the function of IL-17C in NTHi- and cigarette smoke (CS)-induced models of COPD. Neutrophilic inflammation and tissue destruction were decreased in lungs of IL-17C-deficient mice (Il-17c-/-) chronically exposed to NTHi. Numbers of pulmonary neutrophils were decreased in Il-17c-/- mice after acute exposure to the combination of NTHi and CS. However, Il-17c-/- mice were not protected from CS-induced lung inflammation. In a preliminary patient study, we show that IL-17C is present in sputum samples obtained during AECOPD and associates with disease severity. Concentrations of IL-17C were significantly increased during advanced COPD (GOLD III/IV) compared to moderate COPD (GOLD I/II). Concentrations of IL-17A and IL-17E did not associate with disease severity. Our data suggest that IL-17C promotes harmful pulmonary inflammation triggered by bacteria in COPD.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1932-6203eISSN: 1932-6203DOI: 10.1371/journal.pone.0243484Titel-ID: cdi_plos_journals_2476219383
- Format
- –
- Schlagworte
- Acute Disease, Aged, Air pollution, Alveoli, Animals, Atmospheric pollution, Bacteria, Biology and Life Sciences, Bronchus, Chemokines, Chronic obstructive pulmonary disease, Cigarette smoke, Cigarette Smoking - adverse effects, Critical care, Cytokines, Cytokines - metabolism, Denaturation, Development and progression, Disease Progression, Experiments, Female, Gene expression, Glyceraldehyde-3-phosphate dehydrogenase, Gram-negative bacteria, Haemophilus influenzae - physiology, Hemophilus influenzae, Humans, Immune system, Indoor air, Indoor air pollution, Indoor air quality, Indoor environments, Inflammation, Interleukin 6, Interleukin-17 - metabolism, Internal medicine, Lung - microbiology, Lung - pathology, Lung diseases, Lung diseases, Obstructive, Lungs, Male, Medicine, Medicine and Health Sciences, Mice, Mice, Inbred C57BL, Neutrophils, Neutrophils - pathology, Obstructive lung disease, Outdoor air quality, Pneumonia - microbiology, Polymerase chain reaction, Pulmonary Disease, Chronic Obstructive - microbiology, R&D, Research & development, Research facilities, Respiratory function, Risk analysis, Risk factors, Smoke, Sputum, Sputum - microbiology, Streptococcus infections, Trachea, Trinucleotide repeats