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Deutscher Rheumatologiekongress 2020, 48. Kongress der Deutschen Gesellschaft für Rheumatologie (DGRh), 34. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie (DGORh)

09.09. - 12.09.2020, virtuell

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Vascular smooth muscle cells of human aorta express CXCL17 – a possible mechanism for cell recruitment in GCA

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  • Anna Luise Kernder - Poliklinik und Funktionsbereich für Rheumatologie & Hiller Forschungszentrum, Heinrich-Heine-Universität, Düsseldorf
  • Johanna Mucke - Poliklinik und Funktionsbereich für Rheumatologie & Hiller Forschungszentrum, Heinrich-Heine-Universität, Düsseldorf
  • Long Tang-Chieu - Poliklinik und Funktionsbereich für Rheumatologie & Hiller Forschungszentrum, Heinrich-Heine-Universität, Düsseldorf
  • Dennis Bleck - Poliklinik und Funktionsbereich für Rheumatologie & Hiller Forschungszentrum, Heinrich-Heine-Universität, Düsseldorf
  • Torsten Lowin - Poliklinik und Funktionsbereich für Rheumatologie & Hiller Forschungszentrum, Heinrich-Heine-Universität, Düsseldorf
  • Payam Akhyari - Klinik für Herzchirurgie, Heinrich-Heine-Universität, Düsseldorf
  • Ellen Bleck - Poliklinik und Funktionsbereich für Rheumatologie & Hiller Forschungszentrum, Heinrich-Heine-Universität, Düsseldorf
  • Claudia Heier - Poliklinik und Funktionsbereich für Rheumatologie & Hiller Forschungszentrum, Heinrich-Heine-Universität, Düsseldorf
  • Georg Pongratz - Poliklinik und Funktionsbereich für Rheumatologie & Hiller Forschungszentrum, Heinrich-Heine-Universität, Düsseldorf
  • Matthias Schneider - Poliklinik und Funktionsbereich für Rheumatologie & Hiller Forschungszentrum, Heinrich-Heine-Universität, Düsseldorf
  • Stefan Vordenbäumen - Klinik für Herzchirurgie, Heinrich-Heine-Universität, Düsseldorf

Deutsche Gesellschaft für Rheumatologie. Deutsche Gesellschaft für Orthopädische Rheumatologie. Deutscher Rheumatologiekongress 2020, 48. Kongress der Deutschen Gesellschaft für Rheumatologie (DGRh), 34. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie (DGORh). sine loco [digital], 09.-12.09.2020. Düsseldorf: German Medical Science GMS Publishing House; 2020. DocET.13

doi: 10.3205/20dgrh035, urn:nbn:de:0183-20dgrh0352

Published: September 9, 2020

© 2020 Kernder et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at http://creativecommons.org/licenses/by/4.0/.

Outline

Text

Introduction: Giant cell arteritis (GCA) is characterized by an increased release of IFN-γ by Th1 cells and dendritic cells accompanied by an invasion of lymphocytes, dendritic cells and monocytes. The mechanisms contributing to cellular trafficking in GCA are incompletely understood. The most recently discovered chemokine CXCL17 is known to attract monocytes and dendritic cells. CXCL17 and its putative receptor GPR35 have not been assessed in GCA so far. We therefore analyzed the expression and regulation of CXCL17 and GPR35 in human aorta.

Methods: Aortic specimens from patients undergoing cardiac operations were used for CXCL17 immunohistochemistry and isolation of vascular smooth muscle cells (SMC, Tunica media). Before staining, pieces were incubated in medium w/o IFN-γ over night. CXCL17 and GPR35 expression of cultured SMC and human umbilical vein endothelial cells (HUVECs) was quantified by qPCR and ELISA (after stimulation with IFN-γ, TNF-α, IL1-β). In situ-hydridization/immunfluorescence double staining was used to localize CXCL17-mRNA in tissue.

Results: CXCL17 and GPR35 are widely expressed in human aortic pieces after stimulation with IFN-γ. CXCL17-mRNA was located to the tunica media of the arterial wall (vascular smooth muscle cells). In SMC culture, CXCL17-mRNA and protein production was further upregulated by IFN-γ (7-fold, p=0.02 and 3,7 fold, p<0.001). Endothelial cells (HUVECs) in culture did not express CXCL17. The receptor of CXCL17, GPR35, was detected in HUVECs und SMC by qPCR and immunohistochemistry.

Conclusion: CXCL17 and GPR35 are abundant in human aorta. The expression of CXCL17 by SMC in the tunica media is induced by IFN-γ. Therefore the chemokine and its receptor may constitute a hitherto unrecognized regulatory mechanism for the recruitment of inflammatory cells in GCA characterized by an increased release of IFN-γ by Th1 cells and dendritic cells. Further research is needed to better understand this mechanism and possibly define new therapeutic targets.

Disclosures: None declared