Simple view
Full metadata view
Authors
Statistics
Cigarette smoke-exposed neutrophils die unconventionally but are rapidly phagocytosed by macrophages
cell death
monocytes/macrophages
neutrophils
phagocytosis
scavenger receptors
tobacco smoke
Pulmonary accumulation of neutrophils is typical for active smokers who are also predisposed to multiple inflammatory and infectious lung diseases. We show that human neutrophil exposure to cigarette smoke extract (CSE) leads to an atypical cell death sharing features of apoptosis, autophagy and necrosis. Accumulation of tar-like substances in autophagosomes is also apparent. Before detection of established cell death markers, CSE-treated neutrophils are effectively recognized and non-phlogistically phagocytosed by monocyte-derived macrophages. Blockade of LOX-1 and scavenger receptor A, but not MARCO or CD36, as well as pre-incubation with oxLDL, inhibited phagocytosis, suggesting that oxLDL-like structures are major phagocytosis signals. Specific lipid (\beta-carotene and quercetin), but not aqueous, antioxidants increased the pro-phagocytic effects of CSE. In contrast to non-phlogistic phagocytosis, degranulation of secondary granules, as monitored by lactoferrin release, was apparent on CSE exposure, which is likely to promote pulmonary inflammation and tissue degradation. Furthermore, CSE-exposed neutrophils exhibited a compromised ability to ingest the respiratory pathogen, Staphylococcus aureus, which likely contributes to bacterial persistence in the lungs of smokers and is likely to promote further pulmonary recruitment of neutrophils. These data provide mechanistic insight into the lack of accumulation of apoptotic neutrophil populations in the lungs of smokers and their increased susceptibility to degradative pulmonary diseases and bacterial infections.
dc.abstract.en | Pulmonary accumulation of neutrophils is typical for active smokers who are also predisposed to multiple inflammatory and infectious lung diseases. We show that human neutrophil exposure to cigarette smoke extract (CSE) leads to an atypical cell death sharing features of apoptosis, autophagy and necrosis. Accumulation of tar-like substances in autophagosomes is also apparent. Before detection of established cell death markers, CSE-treated neutrophils are effectively recognized and non-phlogistically phagocytosed by monocyte-derived macrophages. Blockade of LOX-1 and scavenger receptor A, but not MARCO or CD36, as well as pre-incubation with oxLDL, inhibited phagocytosis, suggesting that oxLDL-like structures are major phagocytosis signals. Specific lipid (\beta-carotene and quercetin), but not aqueous, antioxidants increased the pro-phagocytic effects of CSE. In contrast to non-phlogistic phagocytosis, degranulation of secondary granules, as monitored by lactoferrin release, was apparent on CSE exposure, which is likely to promote pulmonary inflammation and tissue degradation. Furthermore, CSE-exposed neutrophils exhibited a compromised ability to ingest the respiratory pathogen, Staphylococcus aureus, which likely contributes to bacterial persistence in the lungs of smokers and is likely to promote further pulmonary recruitment of neutrophils. These data provide mechanistic insight into the lack of accumulation of apoptotic neutrophil populations in the lungs of smokers and their increased susceptibility to degradative pulmonary diseases and bacterial infections. | pl |
dc.affiliation | Wydział Biochemii, Biofizyki i Biotechnologii : Zakład Immunologii | pl |
dc.affiliation | Wydział Biochemii, Biofizyki i Biotechnologii : Zakład Mikrobiologii | pl |
dc.contributor.author | Guzik, Krzysztof - 128253 | pl |
dc.contributor.author | Skret, J. | pl |
dc.contributor.author | Smagur, Jan | pl |
dc.contributor.author | Bzowska, Małgorzata - 127506 | pl |
dc.contributor.author | Gajkowska, B. | pl |
dc.contributor.author | Scott, DA | pl |
dc.contributor.author | Potempa, Jan - 131531 | pl |
dc.date.accessioned | 2018-11-02T17:27:56Z | |
dc.date.available | 2018-11-02T17:27:56Z | |
dc.date.issued | 2011 | pl |
dc.date.openaccess | 0 | |
dc.description.accesstime | w momencie opublikowania | |
dc.description.version | ostateczna wersja wydawcy | |
dc.description.volume | 2 | pl |
dc.identifier.articleid | e131 | pl |
dc.identifier.doi | 10.1038/cddis.2011.13 | pl |
dc.identifier.eissn | 2041-4889 | pl |
dc.identifier.project | ROD UJ / OP | pl |
dc.identifier.uri | https://ruj.uj.edu.pl/xmlui/handle/item/59278 | |
dc.language | eng | pl |
dc.language.container | eng | pl |
dc.rights | Udzielam licencji. Uznanie autorstwa - Użycie niekomercyjne - Na tych samych warunkach 3.0 Polska | * |
dc.rights.licence | CC-BY-NC-SA | |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-sa/3.0/pl/legalcode | * |
dc.share.type | otwarte czasopismo | |
dc.subject.en | cell death | pl |
dc.subject.en | monocytes/macrophages | pl |
dc.subject.en | neutrophils | pl |
dc.subject.en | phagocytosis | pl |
dc.subject.en | scavenger receptors | pl |
dc.subject.en | tobacco smoke | pl |
dc.subtype | Article | pl |
dc.title | Cigarette smoke-exposed neutrophils die unconventionally but are rapidly phagocytosed by macrophages | pl |
dc.title.journal | Cell Death and Disease | pl |
dc.type | JournalArticle | pl |
dspace.entity.type | Publication |
* The migration of download and view statistics prior to the date of April 8, 2024 is in progress.
Views
2
Views per month
Views per city
Downloads
Open Access