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AuthorLackner, Inadc.contributor.author
AuthorWeber, Birtedc.contributor.author
AuthorBaur, Meikedc.contributor.author
AuthorFois, Giorgiodc.contributor.author
AuthorGebhard, Floriandc.contributor.author
AuthorPfeifer, Romandc.contributor.author
AuthorCinelli, Paolodc.contributor.author
AuthorHalvachizadeh, Saschadc.contributor.author
AuthorLipiski, Miriamdc.contributor.author
AuthorCesarovic, Nikoladc.contributor.author
AuthorSchrezenmeier, Hubertdc.contributor.author
AuthorHuber-Lang, Markusdc.contributor.author
AuthorPape, Hans-Christophdc.contributor.author
AuthorKalbitz, Miriamdc.contributor.author
Date of accession2021-04-19T14:08:23Zdc.date.accessioned
Available in OPARU since2021-04-19T14:08:23Zdc.date.available
Date of first publication2020-01-31dc.date.issued
AbstractBackground: The complement system is part of the innate immunity, is activated immediately after trauma and is associated with adult respiratory distress syndrome, acute lung injury, multiple organ failure, and with death of multiply injured patients. The aim of the study was to investigate the complement activation in multiply injured pigs as well as its effects on the heart in vivo and in vitro. Moreover, the impact of reamed vs. non-reamed intramedullary nailing was examined with regard to the complement activation after multiple trauma in pigs. Materials and Methods: Male pigs received multiple trauma, followed by femoral nailing with/without prior conventional reaming. Systemic complement hemolytic activity (CH-50 and AH-50) as well as the local cardiac expression of C3a receptor, C5a receptors1/2, and the deposition of the fragments C3b/iC3b/C3c was determined in vivo after trauma. Human cardiomyocytes were exposed to C3a or C5a and analyzed regarding calcium signaling and mitochondrial respiration. Results: Systemic complement activation increased within 6 h after trauma and was mediated via the classical and the alternative pathway. Furthermore, complement activation correlated with invasiveness of fracture treatment. The expression of receptors for complement activation were altered locally in vivo in left ventricles. C3a and C5a acted detrimentally on human cardiomyocytes by affecting their functionality and their mitochondrial respiration in vitro. Conclusion: After multiple trauma, an early activation of the complement system is triggered, affecting the heart in vivo as well as in vitro, leading to complement-induced cardiac dysfunction. The intensity of complement activation after multiple trauma might correlate with the invasiveness of fracture treatment. Reaming of the femoral canal might contribute to an enhanced “second hit” response after trauma. Consequently, the choice of fracture treatment might imply the clinical outcome of the critically injured patients and might be therefore crucial for their survival.dc.description.abstract
Languageendc.language.iso
PublisherUniversität Ulmdc.publisher
LicenseCC BY 4.0 Internationaldc.rights
Link to license texthttps://creativecommons.org/licenses/by/4.0/dc.rights.uri
Keywordcardiac dysfunctiondc.subject
Keywordfemoral nailingdc.subject
Keywordconventional reamingdc.subject
Dewey Decimal GroupDDC 610 / Medicine & healthdc.subject.ddc
MeSHMultiple traumadc.subject.mesh
MeSHInflammationdc.subject.mesh
MeSHFracture fixation, Intramedullarydc.subject.mesh
MeSHComplement activationdc.subject.mesh
MeSHMyocytes, Cardiacdc.subject.mesh
TitleComplement activation and organ damage after trauma—differential immune response based on surgical treatment strategydc.title
Resource typeWissenschaftlicher Artikeldc.type
SWORD Date2020-01-31T06:39:54Zdc.date.updated
VersionpublishedVersiondc.description.version
DOIhttp://dx.doi.org/10.18725/OPARU-36755dc.identifier.doi
URNhttp://nbn-resolving.de/urn:nbn:de:bsz:289-oparu-36817-9dc.identifier.urn
GNDTraumadc.subject.gnd
GNDEntzündungdc.subject.gnd
GNDKomplement <Immunologie>dc.subject.gnd
InstitutionUKU. Klinik für Unfall-, Hand-, Plastische- und Wiederherstellungschirurgieuulm.affiliationSpecific
InstitutionInstitut für Allgemeine Physiologieuulm.affiliationSpecific
InstitutionInstitut für Klinische Transfusionsmedizin und Immungenetik Ulm gGmbH (IKT)uulm.affiliationSpecific
InstitutionUKU. Institut für Klinische und Experimentelle Trauma-Immunologieuulm.affiliationSpecific
Peer reviewjauulm.peerReview
DCMI TypeCollectionuulm.typeDCMI
CategoryPublikationenuulm.category
In cooperation withUniversitätsspital Zürichuulm.cooperation
In cooperation withDRK-Blutspendedienst Baden-Württemberg - Hessenuulm.cooperation
DOI of original publication10.3389/fimmu.2020.00064dc.relation1.doi
Source - Title of sourceFrontiers in Immunologysource.title
Source - Place of publicationFrontiers Mediasource.publisher
Source - Volume11source.volume
Source - Year2020source.year
Source - Article number64source.articleNumber
Source - eISSN1664-3224source.identifier.eissn
Bibliographyuulmuulm.bibliographie
DFG project uulmSFB 1149 / Gefahrenantwort, Störfaktoren und regeneratives Potential nach akutem Trauma / DFG / 251293561uulm.projectDFG
DFG project uulmSFB 1149 Teilprojekt A01 / Späte Schrankenstörung nach experimentellem und klinischem Polytrauma / DFG / 251293561uulm.projectDFG
DFG project uulmSFB 1149 Teilprojekt C07 / Herzfunktion nach Trauma und MSC-basierten regenerativen Strategien / DFG / 251293561uulm.projectDFG
xmlui.metadata.uulm.OAfundingGefördert vom Ministerium für Wissenschaft, Forschung und Kunst Baden-Württemberguulm.OAfunding
xmlui.metadata.uulm.OAfundingOpen-Access-Förderung durch die Medizinische Fakultät der Universität Ulmuulm.OAfunding


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