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The anti-inflammatory peptide Catestatin blocks chemotaxis

View ORCID ProfileElke M. Muntjewerff, Kristel Parv, Sushil K. Mahata, Mia Phillipson, Gustaf Christoffersson, Geert van den Bogaart
doi: https://doi.org/10.1101/2020.11.23.393934
Elke M. Muntjewerff
1Department of Tumor Immunology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, the Netherlands
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  • ORCID record for Elke M. Muntjewerff
Kristel Parv
2Department of Medical Cell biology, Uppsala University, Uppsala, Sweden
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Sushil K. Mahata
3VA San Diego Healthcare System, University of California San Diego, La Jolla, California, USA
4Department of Medicine, University of California San Diego, La Jolla, California, USA
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Mia Phillipson
2Department of Medical Cell biology, Uppsala University, Uppsala, Sweden
5Science for Life Laboratory, Uppsala University, Uppsala, Sweden
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Gustaf Christoffersson
2Department of Medical Cell biology, Uppsala University, Uppsala, Sweden
5Science for Life Laboratory, Uppsala University, Uppsala, Sweden
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  • For correspondence: g.van.den.bogaart@rug.nl gustaf.christoffersson@scilifelab.uu.se
Geert van den Bogaart
1Department of Tumor Immunology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, the Netherlands
6Department of Molecular Immunology and Microbiology, Groningen Biomolecular Sciences and Biotechnology Institute, University of Groningen, Groningen, the Netherlands
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  • For correspondence: g.van.den.bogaart@rug.nl gustaf.christoffersson@scilifelab.uu.se
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Abstract

Increased levels of the anti-inflammatory peptide catestatin (CST), a cleavage product of the pro-hormone chromogranin A, correlates with less severe outcomes in hypertension, colitis and diabetes. However, it is unknown how CST reduces the infiltration of monocytes and macrophages in inflamed tissues. Here, we report that CST blocks leukocyte migration towards inflammatory chemokines. By in vitro and in vivo migration assays, we show that although CST itself is weakly chemotactic, it blocks migration of monocytes and granulocytes to inflammatory attracting factor CC-chemokine ligand 2 (CCL2) and macrophage inflammatory protein 2 (MIP-2). Moreover, it directs CX3CR1+ macrophages away from pancreatic islets. These findings support the emerging notion that CST is a key anti-inflammatory modulator.

Competing Interest Statement

The authors have declared no competing interest.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission.
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Posted November 24, 2020.
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The anti-inflammatory peptide Catestatin blocks chemotaxis
Elke M. Muntjewerff, Kristel Parv, Sushil K. Mahata, Mia Phillipson, Gustaf Christoffersson, Geert van den Bogaart
bioRxiv 2020.11.23.393934; doi: https://doi.org/10.1101/2020.11.23.393934
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The anti-inflammatory peptide Catestatin blocks chemotaxis
Elke M. Muntjewerff, Kristel Parv, Sushil K. Mahata, Mia Phillipson, Gustaf Christoffersson, Geert van den Bogaart
bioRxiv 2020.11.23.393934; doi: https://doi.org/10.1101/2020.11.23.393934

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