Gutenberg Open Science: Death of monocytes through oxidative burst of macrophages and neutrophils : killing in trans

Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-7991

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DC Field	Value	Language
dc.contributor.author	Ponath, Viviane	-
dc.contributor.author	Kaina, Bernd	-
dc.date.accessioned	2022-10-13T10:18:12Z	-
dc.date.available	2022-10-13T10:18:12Z	-
dc.date.issued	2017
dc.identifier.uri	https://openscience.ub.uni-mainz.de/handle/20.500.12030/8006	-
dc.description.abstract	Monocytes and their descendants, macrophages, play a key role in the defence against pathogens. They also contribute to the pathogenesis of inflammatory diseases. Therefore, a mechanism maintaining a balance in the monocyte/macrophage population must be postulated. Our previous studies have shown that monocytes are impaired in DNA repair, rendering them vulnerable to genotoxic stress while monocyte-derived macrophages are DNA repair competent and genotoxic stress-resistant. Based on these findings, we hypothesized that monocytes can be selectively killed by reactive oxygen species (ROS) produced by activated macrophages. We also wished to know whether monocytes and macrophages are protected against their own ROS produced following activation. To this end, we studied the effect of the ROS burst on DNA integrity, cell death and differentiation potential of monocytes. We show that monocytes, but not macrophages, stimulated for ROS production by phorbol-12-myristate-13-acetate (PMA) undergo apoptosis, despite similar levels of initial DNA damage. Following co-cultivation with ROS producing macrophages, monocytes displayed oxidative DNA damage, accumulating DNA single-strand breaks and a high incidence of apoptosis, reducing their ability to give rise to new macrophages. Killing of monocytes by activated macrophages, termed killing in trans, was abolished by ROS scavenging and was also observed in monocytes co-cultivated with ROS producing activated granulocytes. The data revealed that monocytes, which are impaired in the repair of oxidised DNA lesions, are vulnerable to their own ROS and ROS produced by macrophages and granulocytes and support the hypothesis that this is a mechanism regulating the amount of monocytes and macrophages in a ROS-enriched inflammatory environment.	en_GB
dc.description.sponsorship	DFG, Open Access-Publizieren Universität Mainz / Universitätsmedizin	de
dc.language.iso	eng	de
dc.rights	CC BY	*
dc.rights.uri	https://creativecommons.org/licenses/by/4.0/	*
dc.subject.ddc	610 Medizin	de_DE
dc.subject.ddc	610 Medical sciences	en_GB
dc.title	Death of monocytes through oxidative burst of macrophages and neutrophils : killing in trans	en_GB
dc.type	Zeitschriftenaufsatz	de
dc.identifier.doi	http://doi.org/10.25358/openscience-7991	-
jgu.type.dinitype	article	en_GB
jgu.type.version	Published version	de
jgu.type.resource	Text	de
jgu.organisation.department	FB 04 Medizin	de
jgu.organisation.number	2700	-
jgu.organisation.name	Johannes Gutenberg-Universität Mainz	-
jgu.rights.accessrights	openAccess	-
jgu.journal.title	PLOS ONE	de
jgu.journal.volume	12	de
jgu.journal.issue	1	de
jgu.pages.alternative	e0170347	de
jgu.publisher.year	2017	-
jgu.publisher.name	PLOS	de
jgu.publisher.place	San Francisco, California, US	de
jgu.publisher.uri	http://dx.doi.org/10.1371/journal.pone.0170347	de
jgu.publisher.issn	1932-6203	de
jgu.organisation.place	Mainz	-
jgu.subject.ddccode	610	de
opus.date.modified	2018-03-15T10:25:30Z
opus.subject.dfgcode	00-000
opus.organisation.string	FB 04: Medizin: Institut für Toxikologie	de_DE
opus.identifier.opusid	57975
opus.institute.number	0414
opus.metadataonly	false
opus.type.contenttype	Keine	de_DE
opus.type.contenttype	None	en_EN
opus.affiliated	Kaina, Bernd
jgu.publisher.doi	10.1371/journal.pone.0170347	de
jgu.organisation.ror	https://ror.org/023b0x485	-
Appears in collections:	DFG-OA-Publizieren (2012 - 2017)

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