|Janina Łucja Grzegorczyk, Maciej Chałubiński, Aneta Grzelak, Marzanna Jarzębska, Marek L. Kowalski|
Introduction. Immune cells reaching the inflammatory site secrete chemokines such as CC family chemokines (MCP-1,2,3,4, MIP-1 alpha and RANTES) and eotaxin, which are engaged in the signal transmission: cell-cell and cell-matrix. It has been shown that signals transmitted through CCR2 receptor lead to the decrease of inflammatory cells progenitors’ proliferation, but, on the other hand, can increase their survival
Aim of the study. The aim of the study was to compare CCR2 expression on PBMCs (lymphocytes and monocytes) in allergic patients and healthy donors in the context of cell apoptosis.
Material and methods. Mononuclear cells were isolated from peripheral blood of 10 patients with asthma and/or allergic rhinitis and 9 healthy non-atopic donors without any symptoms of airway disease. CCR2 expression and apoptosis were analyzed using flow cytometer. MCP-1 and IL-2 concentrations were analyzed in supernatants using ELISA method.
Results. In allergic patients, CCR2 expression on PBMCs and on monocytes was significantly higher than in healthy subjects. PHA and LPS increased CCR2 expression on PBMCs and lymphocytes after 48 hours of incubation and this enhancement was significantly higher in allergic patients than in healthy donors. The percentage of apoptotic PBMCs in non-stimulated as well as LPS-induced cultures was significantly higher in allergic patients as compared to healthy subjects. The correlation between CCR2 expression and apoptosis of non-stimulated PBMCs has been observed.
Conclusion. CCR2 receptor may be involved in the pathogenesis of allergic inflammation.
keywords: receptor CCR2, alergia, chemokiny, IL-2, MCP-1, apoptoza, CCR-2, chemokines, MCP-1, IL-2, allergy, apoptosis
pages: from 210 to 220
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