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Evidence for the regulation of levels of plasma adhesion molecules by proinflammatory cytokines and their soluble receptors in type 1 diabetes
. Mohamed‐Ali V, Armstrong L, Clarke D, Bolton CH, Pinkney JH (University College London Medical School, Whittington Hospital, London; University Department of Medicine, Southmead Hospital, Bristol; and Clinical Sciences Centre, University Hospital Aintree, Liverpool, UK). Evidence for the regulatio...
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Published in: | Journal of internal medicine 2001-11, Vol.250 (5), p.415-421 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
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Online Access: | Get full text |
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Summary: | . Mohamed‐Ali V, Armstrong L, Clarke D, Bolton CH, Pinkney JH (University College London Medical School, Whittington Hospital, London; University Department of Medicine, Southmead Hospital, Bristol; and Clinical Sciences Centre, University Hospital Aintree, Liverpool, UK). Evidence for the regulation of levels of plasma adhesion molecules by proinflammatory cytokines and their soluble receptors in type 1 diabetes. J Intern Med 2001; 250: 415–421.
Objectives. To investigate the regulation of soluble adhesion molecules by tumour necrosis factor‐α (TNF‐α) and interleukin‐6 (IL‐6), and relationships with circulating cytokine receptors, in vivo, in type 1 diabetes.
Design. Cross‐sectional study.
Setting. University hospital diabetes clinic.
Subjects. A total of 47 non‐nephropathic, Caucasian type 1 diabetics and 39 nondiabetic controls.
Outcome measures. Plasma levels of TNF‐α, IL‐6, their soluble receptors and adhesion molecules intercellular adhesion molecule‐1 (sICAM‐1), vascular cell adhesion molecule‐1 (sVCAM‐1), sE‐selectin and von Willebrand factor (vWF), and risk factors for cardiovascular disease.
Results. Plasma concentrations of IL‐6 were elevated in diabetic patients compared with controls [median (interquartiles) 1.28 (0.89–2.65) vs. 0.66 (0.45–1.73) pg mL−1: P=0.016], and in these patients IL‐6 and soluble IL‐6 receptor (sIL‐6R) levels correlated with concentrations of sICAM‐1 (r=0.41, P=0.012 and r=0.31, P=0.04, respectively). Tumour necrosis factor‐α soluble receptor‐2 (sTNFRII), but not TNF‐α or tumour necrosis factor soluble receptor‐1 (sTNFRI), was elevated in diabetic subjects (P=0.027). Plasma TNF‐α levels correlated with sVCAM‐1 (r=0.39, P=0.008), triglycerides (r=0.36, P=0.021) and diastolic blood pressure (r=0.35; P=0.024). Both sTNFRI and sTNFRII correlated with blood pressure (r=0.46, P=0.002; r=0.32, P=0.034) and triglycerides (r=0.33, P=0.033; r=0.29, P=0.05). In contrast, HDL‐cholesterol and triglyceride were related to sE‐selectin (r=−0.45 and +0.45; both P |
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ISSN: | 0954-6820 1365-2796 |
DOI: | 10.1046/j.1365-2796.2001.00900.x |