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Cigarette smoke-exposed neutrophils die unconventionally but are rapidly phagocytosed by macrophages

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Cigarette smoke-exposed neutrophils die unconventionally but are rapidly phagocytosed by macrophages

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dc.contributor.author Guzik, Krzysztof [SAP11014380] pl
dc.contributor.author Skret, J. pl
dc.contributor.author Smagur, Jan [USOS58275] pl
dc.contributor.author Bzowska, Małgorzata [SAP11016057] pl
dc.contributor.author Gajkowska, B. pl
dc.contributor.author Scott, DA pl
dc.contributor.author Potempa, Jan [SAP11010833] pl
dc.date.accessioned 2018-11-02T17:27:56Z
dc.date.available 2018-11-02T17:27:56Z
dc.date.issued 2011 pl
dc.identifier.uri https://ruj.uj.edu.pl/xmlui/handle/item/59278
dc.language eng pl
dc.rights Udzielam licencji. Uznanie autorstwa - Użycie niekomercyjne - Na tych samych warunkach 3.0 Polska *
dc.rights.uri http://creativecommons.org/licenses/by-nc-sa/3.0/pl/legalcode *
dc.title Cigarette smoke-exposed neutrophils die unconventionally but are rapidly phagocytosed by macrophages pl
dc.type JournalArticle pl
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.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.description.volume 2 pl
dc.identifier.doi 10.1038/cddis.2011.13 pl
dc.identifier.eissn 2041-4889 pl
dc.title.journal Cell Death and Disease pl
dc.language.container eng pl
dc.affiliation Wydział Biochemii, Biofizyki i Biotechnologii : Zakład Immunologii pl
dc.affiliation Wydział Biochemii, Biofizyki i Biotechnologii : Zakład Mikrobiologii pl
dc.subtype Article pl
dc.identifier.articleid e131 pl
dc.rights.original CC-BY-NC-SA; otwarte czasopismo; ostateczna wersja wydawcy; w momencie opublikowania; 0 pl
dc.identifier.project ROD UJ / OP pl


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Udzielam licencji. Uznanie autorstwa - Użycie niekomercyjne - Na tych samych warunkach 3.0 Polska Except where otherwise noted, this item's license is described as Udzielam licencji. Uznanie autorstwa - Użycie niekomercyjne - Na tych samych warunkach 3.0 Polska