Document Detail


Endovascular aneurysm repair reverses the increased titer and the inflammatory activity of interleukin-1α in the serum of patients with abdominal aortic aneurysm.
MedLine Citation:
PMID:  21620624     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: To examine serum cytokine/chemokine profiles before and 6 months after endovascular repair (EVAR) of abdominal aortic aneurysm (AAA) and to determine whether they correlate with serum inflammatory activity using an in vitro model of leukocyte recruitment.
METHODS: Serum IL-1-α, IL-1β, IL-4, IL-6, IL-8, IL-10, IFN-γ, IP-10, MCP-1, TNF-α, and TNF-β were measured using a cytometry-based immunoassay. To test patient serum for direct inflammatory activity, human endothelial cells (EC) were stimulated with 30% patient serum for 24 hours. To test patient serum for the ability to prime EC for inflammatory responses, EC were incubated with 30% patient serum for 24 hours, followed by stimulation with low-dose (5 U/mL) TNF for 4 hours. Under both regimens of stimulation, the degree of EC activation was assessed by assaying neutrophil recruitment in a flow-based model.
RESULTS: Only IL-1α (67.9 ± 10.4 pg/mL vs 41.9 ± 7.4 pg/mL) and IL-8 (51.5 ± 5.1 vs 32.6 ± 4.7 pg/mL) changed significantly after surgery. Patient serum alone was unable to activate EC. However, serum from both time points could prime EC responses to low-dose TNF. Thus, after priming with preoperative serum, EC stimulated with TNF could recruit 76.7 ± 12.0 neutrophils/mm(2) into the subendothelial cell space. Post-EVAR serum was significantly less effective (44.4 ± 10.2 neutrophils/mm(2)). This reduction in neutrophil recruitment correlated with reduced IL-1α in post-EVAR serum. The addition of a neutralizing antibody against IL-1α to pre-EVAR serum inhibited EC priming and neutrophil recruitment, strongly implying that this cytokine was the priming agent.
CONCLUSION: EVAR reduces serum IL-1α and its inflammatory activity in patient serum. IL-1α is, therefore, implicated in the molecular pathology of AAAs and may have potential as a clinically useful biomarker.
Authors:
Clara M Yates; Mohamed Abdelhamid; Donald J Adam; Gerard B Nash; Andrew W Bradbury; G Ed Rainger
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-05-28
Journal Detail:
Title:  Journal of vascular surgery     Volume:  54     ISSN:  1097-6809     ISO Abbreviation:  J. Vasc. Surg.     Publication Date:  2011 Aug 
Date Detail:
Created Date:  2011-08-08     Completed Date:  2011-10-24     Revised Date:  2012-10-03    
Medline Journal Info:
Nlm Unique ID:  8407742     Medline TA:  J Vasc Surg     Country:  United States    
Other Details:
Languages:  eng     Pagination:  497-503     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Society for Vascular Surgery. Published by Mosby, Inc. All rights reserved.
Affiliation:
School of Clinical and Experimental Medicine, The University of Birmingham, Birmingham, UK.
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MeSH Terms
Descriptor/Qualifier:
Aged
Aged, 80 and over
Analysis of Variance
Aortic Aneurysm, Abdominal / immunology,  radiography,  surgery*
Aortography / methods
Biological Markers / blood
Case-Control Studies
Cell Adhesion
Cells, Cultured
Down-Regulation
Endothelial Cells / immunology
Endovascular Procedures*
England
Humans
Immunoassay
Inflammation Mediators / blood*
Interleukin-1alpha / blood*
Microscopy, Video
Neutrophils / immunology
Time Factors
Tomography, X-Ray Computed
Transendothelial and Transepithelial Migration
Treatment Outcome
Tumor Necrosis Factor-alpha / blood
Chemical
Reg. No./Substance:
0/Biological Markers; 0/Inflammation Mediators; 0/Interleukin-1alpha; 0/Tumor Necrosis Factor-alpha

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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