Neutrophil Elastase and Chronic Lung Disease
Neutrophil elastase (NE) is a major inflammatory protease released by neutrophils and is present in the airways of patients with cystic fibrosis (CF), chronic obstructive pulmonary disease, non-CF bronchiectasis, and bronchopulmonary dysplasia. Although NE facilitates leukocyte transmigration to the...
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| Format: | Article |
| Language: | English |
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MDPI AG
2021-07-01
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| Series: | Biomolecules |
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| Online Access: | https://www.mdpi.com/2218-273X/11/8/1065 |
| _version_ | 1797524603400093696 |
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| author | Judith A. Voynow Meagan Shinbashi |
| author_facet | Judith A. Voynow Meagan Shinbashi |
| author_sort | Judith A. Voynow |
| collection | DOAJ |
| description | Neutrophil elastase (NE) is a major inflammatory protease released by neutrophils and is present in the airways of patients with cystic fibrosis (CF), chronic obstructive pulmonary disease, non-CF bronchiectasis, and bronchopulmonary dysplasia. Although NE facilitates leukocyte transmigration to the site of infection and is required for clearance of Gram-negative bacteria, it also activates inflammation when released into the airway milieu in chronic inflammatory airway diseases. NE exposure induces airway remodeling with increased mucin expression and secretion and impaired ciliary motility. NE interrupts epithelial repair by promoting cellular apoptosis and senescence and it activates inflammation directly by increasing cytokine expression and release, and indirectly by triggering extracellular trap release and exosome release, which magnify protease activity and inflammation in the airway. NE inhibits innate immune function by digesting opsonins and opsonin receptors, degrading innate immune proteins such as lactoferrin, and inhibiting macrophage phagocytosis. Importantly, NE-directed therapies have not yet been effective in preventing the pathologic sequelae of NE exposure, but new therapies are being developed that offer both direct antiprotease activity and multifunctional anti-inflammatory properties. |
| first_indexed | 2024-03-10T08:59:46Z |
| format | Article |
| id | doaj.art-ccb5aea1b79d48fc8da43d95d26eaf4e |
| institution | Directory Open Access Journal |
| issn | 2218-273X |
| language | English |
| last_indexed | 2024-03-10T08:59:46Z |
| publishDate | 2021-07-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Biomolecules |
| spelling | doaj.art-ccb5aea1b79d48fc8da43d95d26eaf4e2023-11-22T06:54:17ZengMDPI AGBiomolecules2218-273X2021-07-01118106510.3390/biom11081065Neutrophil Elastase and Chronic Lung DiseaseJudith A. Voynow0Meagan Shinbashi1Division of Pediatric Pulmonology, Children’s Hospital of Richmond at Virginia Commonwealth University, Richmond, VA 23298, USASchool of Medicine, Virginia Commonwealth University, Richmond, VA 23298, USANeutrophil elastase (NE) is a major inflammatory protease released by neutrophils and is present in the airways of patients with cystic fibrosis (CF), chronic obstructive pulmonary disease, non-CF bronchiectasis, and bronchopulmonary dysplasia. Although NE facilitates leukocyte transmigration to the site of infection and is required for clearance of Gram-negative bacteria, it also activates inflammation when released into the airway milieu in chronic inflammatory airway diseases. NE exposure induces airway remodeling with increased mucin expression and secretion and impaired ciliary motility. NE interrupts epithelial repair by promoting cellular apoptosis and senescence and it activates inflammation directly by increasing cytokine expression and release, and indirectly by triggering extracellular trap release and exosome release, which magnify protease activity and inflammation in the airway. NE inhibits innate immune function by digesting opsonins and opsonin receptors, degrading innate immune proteins such as lactoferrin, and inhibiting macrophage phagocytosis. Importantly, NE-directed therapies have not yet been effective in preventing the pathologic sequelae of NE exposure, but new therapies are being developed that offer both direct antiprotease activity and multifunctional anti-inflammatory properties.https://www.mdpi.com/2218-273X/11/8/1065neutrophil elastasecystic fibrosischronic obstructive pulmonary diseasebronchiectasisbronchopulmonary dysplasiaantiprotease |
| spellingShingle | Judith A. Voynow Meagan Shinbashi Neutrophil Elastase and Chronic Lung Disease Biomolecules neutrophil elastase cystic fibrosis chronic obstructive pulmonary disease bronchiectasis bronchopulmonary dysplasia antiprotease |
| title | Neutrophil Elastase and Chronic Lung Disease |
| title_full | Neutrophil Elastase and Chronic Lung Disease |
| title_fullStr | Neutrophil Elastase and Chronic Lung Disease |
| title_full_unstemmed | Neutrophil Elastase and Chronic Lung Disease |
| title_short | Neutrophil Elastase and Chronic Lung Disease |
| title_sort | neutrophil elastase and chronic lung disease |
| topic | neutrophil elastase cystic fibrosis chronic obstructive pulmonary disease bronchiectasis bronchopulmonary dysplasia antiprotease |
| url | https://www.mdpi.com/2218-273X/11/8/1065 |
| work_keys_str_mv | AT judithavoynow neutrophilelastaseandchroniclungdisease AT meaganshinbashi neutrophilelastaseandchroniclungdisease |