Gutenberg Open Science: ADAMTS-13 regulates neutrophil recruitment in a mouse model of invasive pulmonary aspergillosis

Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-7361

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DC Field	Value	Language
dc.contributor.author	Alflen, Astrid	-
dc.contributor.author	Prüfer, Steve	-
dc.contributor.author	Ebner, Katharina	-
dc.contributor.author	Reuter, Sebastian	-
dc.contributor.author	Lopez, Pamela Aranda	-
dc.contributor.author	Scharrer, Inge	-
dc.contributor.author	Banno, Fumiaki	-
dc.contributor.author	Stassen, Michael	-
dc.contributor.author	Schild, Hansjörg	-
dc.contributor.author	Jurk, Kerstin	-
dc.contributor.author	Bosmann, Markus	-
dc.contributor.author	Beckert, Hendrik	-
dc.contributor.author	Radsak, Markus	-
dc.date.accessioned	2022-07-12T07:22:43Z	-
dc.date.available	2022-07-12T07:22:43Z	-
dc.date.issued	2017
dc.identifier.uri	https://openscience.ub.uni-mainz.de/handle/20.500.12030/7375	-
dc.description.abstract	Von Willebrand factor (VWF) is secreted as an acute phase protein during inflammation. ADAMTS-13 regulates the size and prothrombotic activity of VWF by it’s specific proteolytic activity. To determine the relevance of this regulatory pathway for the innate inflammatory response by polymorphonuclear neutrophils (PMN), we employed a mouse model of invasive pulmonary aspergillosis (IPA) where PMN functionality is crucial for fungal clearance and survival. IPA was induced by intratracheal application of Aspergillus fumigatus (A. fumigatus) conidia in wildtype (129/Sv/Pas) or ADAMTS-13 deficient (Adamts13−/−) mice. While neutropenic mice developed lethal IPA, all wildtype mice survived the infection. In contrast to wildtype or VWF deficient mice, Adamts13−/− mice displayed more severe signs of disease with a lethal course in 24% with an increased fungal burden and signs of acute lung injury. Histology sections demonstrated a more pronounced perivascular leukocyte infiltration in support of a dysregulated inflammatory response in Adamts13−/− mice. Importantly, we observed no general defect in the activation of neutrophil functions in response to conidia or hyphae in vitro. Therefore, we conclude that the proteolytic regulation of VWF by ADAMTS-13 or ADAMTS-13 by itself is an important mechanism to control PMN recruitment in acute inflammatory processes, such as fungal pneumonias.	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	ADAMTS-13 regulates neutrophil recruitment in a mouse model of invasive pulmonary aspergillosis	en_GB
dc.type	Zeitschriftenaufsatz	de
dc.identifier.doi	http://doi.org/10.25358/openscience-7361	-
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	Scientific reports	de
jgu.journal.volume	7	de
jgu.pages.alternative	Art. 7184	de
jgu.publisher.year	2017	-
jgu.publisher.name	Macmillan Publishers Limited, part of Springer Nature	de
jgu.publisher.place	London	de
jgu.publisher.uri	http://dx.doi.org/10.1038/s41598-017-07340-3	de
jgu.publisher.issn	2045-2322	de
jgu.organisation.place	Mainz	-
jgu.subject.ddccode	610	de
opus.date.modified	2018-03-19T10:26:08Z
opus.subject.dfgcode	00-000
opus.organisation.string	FB 04: Medizin: III. Medizinische Klinik und Poliklinik	de_DE
opus.organisation.string	FB 04: Medizin: Institut für Immunologie	de_DE
opus.identifier.opusid	57989
opus.institute.number	0427
opus.institute.number	0412
opus.metadataonly	false
opus.type.contenttype	Keine	de_DE
opus.type.contenttype	None	en_EN
opus.affiliated	Scharrer, Inge
opus.affiliated	Stassen, Michael
opus.affiliated	Schild, Hansjörg
opus.affiliated	Radsak, Markus
jgu.publisher.doi	10.1038/s41598-017-07340-3	de
jgu.organisation.ror	https://ror.org/023b0x485
Appears in collections:	DFG-OA-Publizieren (2012 - 2017)

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