title: Levels of MCP-1 and GM-CSF mRNA correlated with inflammatory cytokines mRNA levels in experimental autoimmune myocarditis in rats.
abstract: Infiltration of monocytes and T cells is known to be an essential trigger for the progression of experimental autoimmune myocarditis (EAM) in rats. Monocyte chemotactic protein-1 (MCP-1) and granulocyte-macrophage colony-stimulating factor (GM-CSF) were shown to mediate the migration of monocytes and T cells into inflammatory sites and to proliferate monocytes. Thus, we evaluated levels of MCP-1 and GM-CSF mRNA in the myocardium of EAM in rats using a real time quantitative PCR method. We also examined the correlation of MCP-1 or GM-CSF mRNA levels with those of inflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and interleukin-6 (IL-6) in the same lesion. Levels of MCP-1, GM-CSF, TNF-alpha, IL-1beta and IL-6 mRNA increased with the progression of myocarditis which was accompanied by the accumulation of ED-1 positive cells. The MCP-1 and GM-CSF mRNA levels were positively correlated with TNF-alpha, IL-1beta and IL-6 mRNA levels in the same lesion of EAM. We also demonstrated that serum MCP-1 concentrations were increased during the active stage of EAM, and were correlated with MCP-1 mRNA levels in the myocardium of each rat. These findings suggest that elevated MCP-1 and GM-CSF may associate with the migration and proliferation of monocytes/macrophages in EAM. Thus, MCP-1 and GM-CSF may play an important role in the progression of EAM.
authors.affiliation: First Department of Internal Medicine, Nara Medical University, Japan.
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Kobayashi
authors.forename: Atsushi
authors.initials: A
authors.lastname: Kubo
authors.forename: Masayuki
authors.initials: M
authors.lastname: Iwano
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Sakaguchi
authors.forename: Kenichi
authors.initials: K
authors.lastname: Samejima
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Kyoda
authors.forename: Kunio
authors.initials: K
authors.lastname: Yonemasu
authors.forename: Toshio
authors.initials: T
authors.lastname: Hashimoto
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases / Q000139:chemically induced / Q000235:genetics* / Q000473:pathology; D018932:Chemokine CCL2 / Q000097:blood / Q000235:genetics*; D016207:Cytokines / Q000235:genetics*; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000235:genetics* / Q000378:metabolism; D007150:Immunohistochemistry; D007249:Inflammation / Q000235:genetics / Q000276:immunology; D008297:Male; D009205:Myocarditis / Q000139:chemically induced / Q000235:genetics* / Q000473:pathology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism*; D051381:Rats; D011917:Rats, Inbred Lew
chemical_list: D018932:Chemokine CCL2; D016207:Cytokines; D012333:RNA, Messenger; D016178:Granulocyte-Macrophage Colony-Stimulating Factor