کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2914865 1575529 2008 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Characterisation of Fractalkine/CX3CL1 and Fractalkine Receptor (CX3CR1) Expression in Abdominal Aortic Aneurysm Disease
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی کاردیولوژی و پزشکی قلب و عروق
پیش نمایش صفحه اول مقاله
Characterisation of Fractalkine/CX3CL1 and Fractalkine Receptor (CX3CR1) Expression in Abdominal Aortic Aneurysm Disease
چکیده انگلیسی

ObjectivesFractalkine (CX3CL1) promotes adhesion and extravasation of leucocytes through interactions with fractalkine receptor (CX3CR1) expressed on CD56+/CD16+ NK cells and CD8+ T cells. The current study aims to test the hypothesis the CX3CL1–CX3CR1 interaction contributes to the inflammatory infiltrate in AAA tissue.Design and methodsImmunohistochemistry (IHC) was used to define expression of CX3CR1 in AAA tissue. Multi-parametric flow cytometry (FC) was used to determine CX3CR1 expression on T-cells (CD3+) and NK cells (CD56+) from AAA tissue and peripheral blood of AAA patients and healthy controls. Regulation of CX3CL1 expression by vascular endothelial (vEC) and smooth muscle cells (vSMC) was examined in vitro using primary cell cultures.ResultsCX3CR1+ cells were detected in 19/28 AAA tissue samples and predominately localised in the adventitia. PBMCs from patients with AAA demonstrated higher percentages of CX3CR1+ NK cells (60.0–88.6%) and T cells (7.5–39.4%) compared with healthy controls. Furthermore, the frequency of CX3CR1+ NK cells (91%) and T cells (94%) in inflammatory AAA tissue were higher than in atherosclerotic AAA tissue. The pro-inflammatory cytokine TNFα increased expression of fractalkine by vSMC and vEC.ConclusionCX3CL1+ and CX3CR1+ cells are present in AAA disease and their interaction may contribute to the recruitment of inflammatory cells seen in AAA tissue.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: European Journal of Vascular and Endovascular Surgery - Volume 36, Issue 1, July 2008, Pages 20–27
نویسندگان
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