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• Troitskaya, M
• Baysa, A
• Vaage, J
• Sand, KL.
• Maghazachi, AA.
• Valen, G
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• Troitskaya, M
• Baysa, A
• Vaage, J
• Sand, KL.
• Maghazachi, AA.
• Valen, G
• [+] on PubMed
• Troitskaya, M
• Baysa, A
• Vaage, J
• Sand, KL.
• Maghazachi, AA.
• Valen, G

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Toxins 2012, 4(12), 1427-1439; doi:10.3390/toxins4121427

Article

Interleukin-17 (IL-17) Expression Is Reduced during Acute Myocardial Infarction: Role on Chemokine Receptor Expression in Monocytes and Their in Vitro Chemotaxis towards Chemokines

Maria Troitskaya ^1,2, Anton Baysa ^1,2, Jarle Vaage ³, Kristin L. Sand ¹, Azzam A. Maghazachi ^1,*  and Guro Valen ^1,2,*

¹ Department of Physiology, Institute of Basic Medical Sciences, University of Oslo, Oslo N-0317, Norway ² Center for Heart Failure Research, University of Oslo, Oslo N-0317, Norway ³ Department of Emergency and Intensive Care at the Institute of Clinical Medicine, Oslo University Hospital, Oslo N-0424, Norway

* Authors to whom correspondence should be addressed.

Received: 15 November 2012; in revised form: 27 November 2012 / Accepted: 28 November 2012 / Published: 30 November 2012

(This article belongs to the Special Issue Toxicity and Therapeutic Interventions in the Immune System)

Download PDF Full-Text [825 KB, uploaded 30 November 2012 14:39 CET]

Abstract: The roles of immune cells and their soluble products during myocardial infarction (MI) are not completely understood. Here, we observed that the percentages of IL-17, but not IL-22, producing cells are reduced in mice splenocytes after developing MI. To correlate this finding with the functional activity of IL-17, we sought to determine its effect on monocytes. In particular, we presumed that this cytokine might affect the chemotaxis of monocytes important for cardiac inflammation and remodeling. We observed that IL-17 tends to reduce the expression of two major chemokine receptors involved in monocyte chemotaxis, namely CCR2 and CXCR4. Further analysis showed that monocytes pretreated with IL-17 have reduced in vitro chemotaxis towards the ligand for CCR2, i.e., MCP-1/CCL2, and the ligand for CXCR4, i.e., SDF-1α/CXCL12. Our results support the possibility that IL-17 may be beneficial in MI, and this could be due to its ability to inhibit the migration of monocytes.

Keywords: myocardial infarction; IL-17; monocytes; chemokines; chemokine receptors

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