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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

by
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.
Toxins 2012, 4(12), 1427-1439; https://doi.org/10.3390/toxins4121427
Submission received: 15 November 2012 / Revised: 27 November 2012 / Accepted: 28 November 2012 / Published: 30 November 2012
(This article belongs to the Collection Toxicity and Therapeutic Interventions in the Immune System)
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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 myocardial infarction; IL-17; monocytes; chemokines; chemokine receptors

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MDPI and ACS Style

Troitskaya, M.; Baysa, A.; Vaage, J.; Sand, K.L.; Maghazachi, A.A.; Valen, G. 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. Toxins 2012, 4, 1427-1439. https://doi.org/10.3390/toxins4121427

AMA Style

Troitskaya M, Baysa A, Vaage J, Sand KL, Maghazachi AA, Valen G. 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. Toxins. 2012; 4(12):1427-1439. https://doi.org/10.3390/toxins4121427

Chicago/Turabian Style

Troitskaya, Maria, Anton Baysa, Jarle Vaage, Kristin L. Sand, Azzam A. Maghazachi, and Guro Valen. 2012. "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" Toxins 4, no. 12: 1427-1439. https://doi.org/10.3390/toxins4121427

APA Style

Troitskaya, M., Baysa, A., Vaage, J., Sand, K. L., Maghazachi, A. A., & Valen, G. (2012). 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. Toxins, 4(12), 1427-1439. https://doi.org/10.3390/toxins4121427

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