Neutrophil Elastase-Mediated Lung Disease
Open accessAbstract
Elastases of both the neutrophil and macrophage have been implicated in lung disease initiation and progression. Although it is unlikely that these proteases evolved for the purpose of injuring lung tissue, the elastin-rich connective tissue framework of the lungs appears to be particularly susceptible to the action of elastolytic proteases. Assuming that neutrophil elastase most likely plays a role in the migration of neutrophils toward a site of inflammation and degradation of proteins from invading organisms or other products of the inflammatory response, it is the role of inhibitors of this protease to protect normal tissues from its effects. In alpha-1 antitrypsin deficiency we find an experiment of nature that disrupts this protease-anti-protease balance, resulting in an increased risk of destructive lung disease.
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HNE is a causal factor in the progression of emphysema and chronic obstructive pulmonary disease (COPD).
“However, HNE is also a causal factor in the progression of emphysema and chronic obstructive pulmonary disease (COPD) [6,7] due to the enzyme’s propensity to propagate cyclic inflammation, recruit neutrophils, and proteolytically destroy elastic lung tissue [8,9].”
From Discrimination of Methionine Sulfoxide and Sulfone by Human Neutrophil Elastase (2021) · cites this paper as [9]
In Historical perspectives (page unavailable), the paper calls HNE a potent emphysema-promoting agent in animal studies and assigns it a prominent pathogenic role in COPD associated with alpha-1 antitrypsin deficiency. Augmentation therapy (page unavailable) describes slowing lung-function decline by protecting lung tissue from proteolytic attack. The claim extends that causal role to COPD generally, whereas the paper says cigarette-smoke-induced lung disease involves additional proteases and pathways. (LLM, conf=0.83)
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Research works printed but not linked: 31
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Cited by
Sorted by citations
Discrimination of Methionine Sulfoxide and Sulfone by Human Neutrophil Elastase
Leahy, D., Grant, C., Jackson, A., Duff, A., Tardiota, N., Van Haeften, J., Chen, X., Peake, J. M., Kruppa, M. D., Smith, E. T., et al. (2021) · Molecules · doi:10.3390/molecules26175344 · Cited by 2 · see citing works
“due to the enzyme’s propensity to propagate cyclic inflammation, recruit neutrophils, and proteolytically destroy elastic lung tissue [8,9].”
Background
- Authors
- Sandhaus, R. A., & Turino, G.
- Affiliations
- National Jewish Health (US)
- Columbia University (US)
- ORCID
- Sandhaus, Robert A.
- Venue
- COPD: Journal of Chronic Obstructive Pulmonary Disease
- Publisher
- Informa UK Limited
- Published
- 2013-03-07
- Volume
- 10
- Issue
- sup1
- Pages
- 60-63
- ISSN
- 1541-2555 (ISSN-L)
- 1541-2563
- OpenAlex
- W2148489542
- Cited by
- 95
- References
- 0
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 3 · 2023: 5 · 2022: 5 · 2021: 7 · 2020: 5 · 2019: 4 · 2018: 6 · 2017: 13 · 2016: 8 · 2015: 13 · 2014: 13 · 2013: 4
- FWCI
- 1.08
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- COPD Journal of Chronic Obstructive Pulmonary Disease (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Protease and Inhibitor Mechanisms
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Keywords
- neutrophil elastase, lung disease, protease-antiprotease balance, alpha-1 antitrypsin deficiency, neutrophil migration, elastin degradation, macrophage elastase, chronic obstructive pulmonary disease
- MeSH terms
- alpha 1-Antitrypsin, Humans, Pulmonary Emphysema, Serine Proteinase Inhibitors, Leukocyte Elastase, alpha 1-Antitrypsin Deficiency
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