title: 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.
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-1&#945;/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.
authors.affiliation: Department of Physiology, Institute of Basic Medical Sciences, University of Oslo, Oslo N-0317, Norway. maria_nemo@mail.ru
authors.forename: Maria
authors.initials: M
authors.lastname: Troitskaya
authors.forename: Anton
authors.initials: A
authors.lastname: Baysa
authors.forename: Jarle
authors.initials: J
authors.lastname: Vaage
authors.forename: Kristin L
authors.initials: KL
authors.lastname: Sand
authors.forename: Azzam A
authors.initials: AA
authors.lastname: Maghazachi
authors.forename: Guro
authors.initials: G
authors.lastname: Valen
mesh_terms: D000818:Animals; D018925:Chemokines / Q000378:metabolism*; D002633:Chemotaxis / Q000187:drug effects*; D020381:Interleukin-17 / Q000494:pharmacology*; D007378:Interleukins / Q000494:pharmacology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009000:Monocytes / Q000187:drug effects* / Q000502:physiology; D009203:Myocardial Infarction / Q000378:metabolism*; D054390:Receptors, CCR2 / Q000378:metabolism; D019718:Receptors, CXCR4 / Q000378:metabolism; D018123:Receptors, Interleukin / Q000378:metabolism; D053722:Receptors, Interleukin-17 / Q000378:metabolism; D013154:Spleen / Q000166:cytology; D000097043:Interleukin-22
chemical_list: D018925:Chemokines; D020381:Interleukin-17; D007378:Interleukins; D054390:Receptors, CCR2; D019718:Receptors, CXCR4; D018123:Receptors, Interleukin; D053722:Receptors, Interleukin-17; D000097043:Interleukin-22; C514936:CXCR4 protein, mouse; C515335:Ccr2 protein, mouse; C415369:interleukin-22 receptor