کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2893362 1172412 2009 10 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Serum amyloid A induction of cytokines in monocytes/macrophages and lymphocytes
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی کاردیولوژی و پزشکی قلب و عروق
پیش نمایش صفحه اول مقاله
Serum amyloid A induction of cytokines in monocytes/macrophages and lymphocytes
چکیده انگلیسی

ObjectivesSerum amyloid A (SAA) is a biomarker of inflammation. Elevated blood levels in cardiovascular disease and local deposition in atheroma implies a role of SAA as a mediator rather than just a marker of inflammation. This study explored SAA-induced cytokine production and secretion by mononuclear cells.Methods and resultsRT-PCR showed that SAA time-dependently induced cytokine mRNAs in peripheral blood mononuclear cells (PBMC) and THP-1 monocytoid cells, and dramatically increased IL-1β, MCP-1, IL-6, IL-8, IL-10, GM-CSF, TNF, and MIP-1α secretion by PBMC to levels 28 to 25,000 fold above baseline, as measured with Bio-Plex kits; monocytes were the principle source. SAA induction of cytokines in monocyte-derived macrophages (MDM) was significantly higher than from monocytes from the same donors. SAA time-dependently induced transient and significant upregulation of NF-κB1 mRNA; inhibitor studies indicate that activation of NF-κB through the ERK1/2, p38 and JNK MAPKs and the PI3K pathway was involved. PBMC from 10 patients with coronary artery disease (CAD) spontaneously secreted higher levels of IL-6 and MIP-1α after 24 h incubation than PBMC from normal controls, whereas SAA-induced levels of all cytokines were similar to controls. Aortic and coronary sinus sampling in 23 CAD patients indicated significant SAA release into the coronary circulation, not evident in 11 controls.ConclusionsSAA can increase monocyte and macrophage cytokine production, possibly at sites of atherosclerosis, thereby contributing to the pro-inflammatory state in coronary artery disease.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Atherosclerosis - Volume 207, Issue 2, December 2009, Pages 374–383
نویسندگان
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