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Clinical Chemistry 50: 226-228, 2004; 10.1373/clinchem.2003.022962
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(Clinical Chemistry. 2004;50:226-228.)
© 2004 American Association for Clinical Chemistry, Inc.

Technical Briefs

Rapid Genotyping for Tumor Necrosis Factor-{alpha} (TNF-{alpha}) -863C/A Promoter Polymorphism That Determines TNF-{alpha} Response

Michael Heesen1,a, Dagmar Kunz2, Martina Wessiepe3, Tom van der Poll4, Aeilko H. Zwinderman5 and Brunhilde Blomeke6

Departments of
1 Anesthesia,
4 Experimental Internal Medicine, and
5 Clinical Epidemiology and Biostatistics, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
Departments of
2 Clinical Chemistry and Pathobiochemistry,
3 Transfusion Medicine, and
6 Dermatology, University Hospital, Aachen, Germany

aaddress correspondence to this author at: Department of Anesthesia, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands; fax 31-20-6979441, e-mail m.heesen@amc.uva.nl

The first 300 words of the full text of this article appear below.

Tumor necrosis factor-{alpha} (TNF-{alpha}) plays a central role in orchestrating the inflammatory response (1). Accordingly, blocking TNF-{alpha} activity has become a standard treatment of several inflammatory diseases (2)(3). TNF-{alpha} production shows high interindividual variations, which have been assigned mainly to inherited factors (4). Several genetic polymorphisms related to TNF-{alpha} synthesis have been detected in the TNF gene (5)(6). The -308 promoter polymorphism was found to affect TNF-{alpha} production by some authors (7) but not by others (8). Similar inconsistencies have been found for the association of this polymorphic site with susceptibility to and/or outcome of sepsis (8)(9). The NcoI polymorphism located within the first intron of the lymphotoxin A (LTA) gene was reported to be associated with TNF-{alpha} plasma concentrations (8). In a recent report, de Jong et al. (10) found no relationship between ex vivo TNF-{alpha} production on endotoxin stimulation of human whole blood and +489, -238, and -376 single-nucleotide polymorphisms or TNFa microsatellites of the TNF-{alpha} gene (10). Thus, the genetic factors determining the TNF-{alpha} response to infection are still poorly defined.

Recently, Skoog et al. (11) identified a C/A exchange at position -863 of the TNF-{alpha} gene promoter and found higher transcriptional activity of the C allele in reporter gene assays. This polymorphic site was found to be associated with thyroid-associated ophthalmopathy (12), Crohn disease(13), juvenile rheumatoid arthritis (14), and the lumbar spine area (15).

In the present study we sought to determine the association of the -863 TNF-{alpha} promoter polymorphism with the TNF-{alpha} production capacity of human blood cells. We describe a new real-time PCR assay with specific . . . [Full Text of this Article]






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