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Titolo:
Macrophage inflammatory protein-1 alpha relates to the recruitment of inflammatory cells in myosin-induced autoimmune myocarditis in rats
Autore:
Toyozaki, T; Saito, T; Shiraishi, H; Tsukamoto, Y; Takano, H; Nagai, T; Hiroshima, K; Ohwada, H; Ishiyama, S; Hiroe, M;
Indirizzi:
Chiba Univ, Sch Med, Inst Pulm Canc Res, Div Pathol, Chiba 2608670, Japan Chiba Univ Chiba Japan 2608670 anc Res, Div Pathol, Chiba 2608670, Japan Chiba Univ, Sch Med, Dept Internal Med 3, Chiba 2608670, Japan Chiba UnivChiba Japan 2608670 Dept Internal Med 3, Chiba 2608670, Japan Tokyo Med & Dent Univ, Dept Med 2, Div Cardiol, Tokyo, Japan Tokyo Med & Dent Univ Tokyo Japan Dept Med 2, Div Cardiol, Tokyo, Japan
Titolo Testata:
LABORATORY INVESTIGATION
fascicolo: 7, volume: 81, anno: 2001,
pagine: 929 - 936
SICI:
0023-6837(200107)81:7<929:MIPART>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
LANGERHANS CELLS; CHEMOKINETIC PROPERTIES; GENE-EXPRESSION; CYTOKINE FAMILY; MESSENGER-RNA; T-CELLS; IN-SITU; MIP-1-ALPHA; DISEASE; HEART;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Toyozaki, T Chiba Univ, Sch Med, Inst Pulm Canc Res, Div Pathol, 1-8-1 Inohana, Chiba 2608670, Japan Chiba Univ 1-8-1 Inohana Chiba Japan 2608670 a 2608670, Japan
Citazione:
T. Toyozaki et al., "Macrophage inflammatory protein-1 alpha relates to the recruitment of inflammatory cells in myosin-induced autoimmune myocarditis in rats", LAB INV, 81(7), 2001, pp. 929-936

Abstract

In experimental autoimmune myocarditis (EAM) there is a characteristic initial focal inflammatory response in the myocardium, induced mainly by CD4(+) T cells and macrophages, which leads to massive myocardial damage. Macrophage inflammatory protein-1 alpha (MIP-1 alpha) induces chemotaxis in lymphocytes, eosinophils, basophils, and macrophages. We assessed the potential role of MIP-I a in the pathogenesis of EAM in rats immunized with porcine myosin. Following immunization, the levels of MIP-1 alpha mRNA in EAM showedan increase on Day 11 and peaked on Day 17. MIP-1 alpha -positive cells were predominantly immunoreactive to OX6 antibody (dendritic cells) and ED2 antibody (resident macrophages) by Day 14. Marked cellular infiltration was seen on Day 17 with the major population of MIP-1 alpha -positive cells also positive for ED1 (inflammatory macrophages). We then examined the association of MIP-1 alpha with the development of myocardial inflammation. Rats were divided into three groups: Group A consisted of EAM rats (n = 10); Group B consisted of EAM rats treated with anti-MIP-1 alpha (1 mg/kg) on Days 11, 13, and 15, before the onset of initial inflammation (n = 5): and Group C consisted of EAM rats treated with anti-MIP-la from the start of the initial inflammation on Days 14, 16, and 18 (n = 5). Rats were euthanized on Day 21 and three transverse sections of the heart were prepared to determine the percentage of the area affected by inflammatory lesions. This area of inflammation was significantly smaller in Group B (27 +/- 4%) than in GroupsA (51 +/- 6%) or C (50 +/- 6%)(p < 0.01), indicating that the administration of antibody before the initiation of inflammation, in part, will inhibitmyocardial inflammation. These data suggest that MIP-1 alpha may play an important role in the recruitment of inflammatory cells in the early stages of EAM.

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Documento generato il 20/01/20 alle ore 21:59:40