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.
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Authors | Maria Troitskaya, Anton Baysa, Jarle Vaage, Kristin L Sand, Azzam A Maghazachi, Guro Valen |
Journal | Toxins
(Toxins (Basel))
Vol. 4
Issue 12
Pg. 1427-39
(Nov 30 2012)
ISSN: 2072-6651 [Electronic] Switzerland |
PMID | 23202375
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- CXCR4 protein, mouse
- Ccr2 protein, mouse
- Chemokines
- Interleukin-17
- Interleukins
- Receptors, CCR2
- Receptors, CXCR4
- Receptors, Interleukin
- Receptors, Interleukin-17
- interleukin-22 receptor
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Topics |
- Animals
- Chemokines
(metabolism)
- Chemotaxis
(drug effects)
- Interleukin-17
(pharmacology)
- Interleukins
(pharmacology)
- Male
- Mice
- Mice, Inbred C57BL
- Monocytes
(drug effects, physiology)
- Myocardial Infarction
(metabolism)
- Receptors, CCR2
(metabolism)
- Receptors, CXCR4
(metabolism)
- Receptors, Interleukin
(metabolism)
- Receptors, Interleukin-17
(metabolism)
- Spleen
(cytology)
- Interleukin-22
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