Murine Macrophages Modulate Their Inflammatory Profile in Response to Gas Plasma-Inactivated Pancreatic Cancer Cells

dc.bibliographicCitation.firstPage2525eng
dc.bibliographicCitation.issue11eng
dc.bibliographicCitation.journalTitleCancerseng
dc.bibliographicCitation.volume13eng
dc.contributor.authorKhabipov, Aydar
dc.contributor.authorFreund, Eric
dc.contributor.authorLiedtke, Kim Rouven
dc.contributor.authorKäding, Andre
dc.contributor.authorRiese, Janik
dc.contributor.authorvan der Linde, Julia
dc.contributor.authorKersting, Stephan
dc.contributor.authorPartecke, Lars-Ivo
dc.contributor.authorBekeschus, Sander
dc.date.accessioned2022-03-23T14:24:43Z
dc.date.available2022-03-23T14:24:43Z
dc.date.issued2021
dc.description.abstractMacrophages and immuno-modulation play a dominant role in the pathology of pancreatic cancer. Gas plasma is a technology recently suggested to demonstrate anticancer efficacy. To this end, two murine cell lines were employed to analyze the inflammatory consequences of plasma-treated pancreatic cancer cells (PDA) on macrophages using the kINPen plasma jet. Plasma treatment decreased the metabolic activity, viability, and migratory activity in an ROS- and treatment time-dependent manner in PDA cells in vitro. These results were confirmed in pancreatic tumors grown on chicken embryos in the TUM-CAM model (in ovo). PDA cells promote tumor-supporting M2 macrophage polarization and cluster formation. Plasma treatment of PDA cells abrogated this cluster formation with a mixed M1/M2 phenotype observed in such co-cultured macrophages. Multiplex chemokine and cytokine quantification showed a marked decrease of the neutrophil chemoattractant CXCL1, IL6, and the tumor growth supporting TGFβ and VEGF in plasma-treated compared to untreated co-culture settings. At the same time, macrophage-attractant CCL4 and MCP1 release were profoundly enhanced. These cellular and secretome data suggest that the plasma-inactivated PDA6606 cells modulate the inflammatory profile of murine RAW 264.7 macrophages favorably, which may support plasma cancer therapy.eng
dc.description.versionpublishedVersioneng
dc.identifier.urihttps://oa.tib.eu/renate/handle/123456789/8337
dc.identifier.urihttps://doi.org/10.34657/7375
dc.language.isoengeng
dc.publisherBasel : MDPIeng
dc.relation.doihttps://doi.org/10.3390/cancers13112525
dc.relation.essn2072-6694
dc.rights.licenseCC BY 4.0 Unportedeng
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/eng
dc.subject.ddc610eng
dc.subject.otherCAPeng
dc.subject.otherPDA6606eng
dc.subject.othercold atmospheric pressure plasmaeng
dc.subject.othercold physical plasmaeng
dc.subject.otherkINPeneng
dc.subject.othermetastasiseng
dc.subject.otherplasma medicineeng
dc.subject.othertumor microenvironment (TME)eng
dc.titleMurine Macrophages Modulate Their Inflammatory Profile in Response to Gas Plasma-Inactivated Pancreatic Cancer Cellseng
dc.typeArticleeng
dc.typeTexteng
tib.accessRightsopenAccesseng
wgl.contributorINPeng
wgl.subjectMedizin, Gesundheiteng
wgl.typeZeitschriftenartikeleng
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