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[Role of innate immunity receptors in development of acute myocardial infarction].
Article en Ru | MEDLINE | ID: mdl-18819410
ABSTRACT

AIM:

To assess influence of toll-like receptors (TLR) ligands on the production of proinflammatory cytokine (TNFalpha) by peripheral blood mononuclear cells in patients with acute myocardial infarction (AMI). MATERIALS AND

METHODS:

Peripheral blood mononuclear cells (PBMC) obtained from 13 patients with AMI on 1st and 14th day and from 17 healthy donors were stimulated by peptidoglycan, poly(IC), lypopolysacchide, zimozan, flagellin and CpG oligodeoxynucleotides, which are ligands of TLR1/2, TLR3, TLR4, TLR2/6, TLR5 and TLR9 respectively. Spontaneous and induced by ligands production of TNFalpha was evaluated in supernatants of PBMC.

RESULTS:

Increased spontaneous production of TNFalpha by PBMC in patients with AIM was revealed on 1st day of the disease. Ligands of TLR2/6 and TLR4 demonstrated marked stimulatory effect on the production of TNFalpha by PBMC in patients with AMI compared with group of healthy subjects.

CONCLUSION:

Increased production of TNFalpha by PBMC in patients with AMI indicates the activation of TLR2 and TLR4 on PBMC. Hyperactivation of TLRs during acute pathologic conditions results in excessive production of proinflammatory cytokines, specifically TNFalpha, and can induce damage of cells and tissues involved in acute pathologic process.
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Factor de Necrosis Tumoral alfa / Receptor Toll-Like 2 / Receptor Toll-Like 4 / Infarto del Miocardio Límite: Aged / Aged80 / Female / Humans / Male / Middle aged Idioma: Ru Revista: Zh Mikrobiol Epidemiol Immunobiol Año: 2008 Tipo del documento: Article
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Factor de Necrosis Tumoral alfa / Receptor Toll-Like 2 / Receptor Toll-Like 4 / Infarto del Miocardio Límite: Aged / Aged80 / Female / Humans / Male / Middle aged Idioma: Ru Revista: Zh Mikrobiol Epidemiol Immunobiol Año: 2008 Tipo del documento: Article