Heterozygous toll-like receptor 4 polymorphism does not influence lipopolysaccharide-induced cytokine release in human whole blood

Sonja Von Aulock, Nicolas W J Schröder, Katja Gueinzius, Stephanie Traub, Sebastian Hoffmann, Kathrin Graf, Stefanie Dimmeler, Thomas Hartung, Ralf R. Schumann, Corinna Hermann

Research output: Contribution to journalArticle

Abstract

The heterozygous Asp299Gly mutation of the toll-like receptor (TLR) 4, the key receptor for lipopoiysaccharide (LPS), has been associated with attenuated inflammatory responses. When 160 healthy volunteers (9% heterozygous and 0.6% homozygous) were genotyped and their LPS-inducible cytokine release was assessed in an ex vivo whole blood test, the responses of heterozygotes did not differ significantly from those of wildtype carriers for any of the cytokines (tumor necrosis factor-α, interleukin [IL]-1β, IL-6, interferon-γ, and granulocyte colony-stimulating factor) or eicosanoids measured or for serum cytokines and C-reactive protein. Ten heterozygous subjects and 12 wild-type control subjects responded similarly to a graded series of LPS and Escherichia coli concentrations, excluding the possibility that allele-specific differences are evident only at low stimulus concentrations or in response to whole pathogens. These data demonstrate that the heterozygous Asp299Gly polymorphism does not exhibit a functional defect in cytokine release after the stimulation of blood monocytes.

Original languageEnglish (US)
Pages (from-to)938-943
Number of pages6
JournalJournal of Infectious Diseases
Volume188
Issue number6
DOIs
StatePublished - Sep 15 2003
Externally publishedYes

Fingerprint

Toll-Like Receptor 4
Lipopolysaccharides
Cytokines
Eicosanoids
Hematologic Tests
Granulocyte Colony-Stimulating Factor
Heterozygote
Interleukin-1
C-Reactive Protein
Interferons
Monocytes
Interleukin-6
Healthy Volunteers
Tumor Necrosis Factor-alpha
Alleles
Escherichia coli
Mutation
Serum

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health
  • Immunology

Cite this

Von Aulock, S., Schröder, N. W. J., Gueinzius, K., Traub, S., Hoffmann, S., Graf, K., ... Hermann, C. (2003). Heterozygous toll-like receptor 4 polymorphism does not influence lipopolysaccharide-induced cytokine release in human whole blood. Journal of Infectious Diseases, 188(6), 938-943. https://doi.org/10.1086/378095

Heterozygous toll-like receptor 4 polymorphism does not influence lipopolysaccharide-induced cytokine release in human whole blood. / Von Aulock, Sonja; Schröder, Nicolas W J; Gueinzius, Katja; Traub, Stephanie; Hoffmann, Sebastian; Graf, Kathrin; Dimmeler, Stefanie; Hartung, Thomas; Schumann, Ralf R.; Hermann, Corinna.

In: Journal of Infectious Diseases, Vol. 188, No. 6, 15.09.2003, p. 938-943.

Research output: Contribution to journalArticle

Von Aulock, S, Schröder, NWJ, Gueinzius, K, Traub, S, Hoffmann, S, Graf, K, Dimmeler, S, Hartung, T, Schumann, RR & Hermann, C 2003, 'Heterozygous toll-like receptor 4 polymorphism does not influence lipopolysaccharide-induced cytokine release in human whole blood', Journal of Infectious Diseases, vol. 188, no. 6, pp. 938-943. https://doi.org/10.1086/378095
Von Aulock, Sonja ; Schröder, Nicolas W J ; Gueinzius, Katja ; Traub, Stephanie ; Hoffmann, Sebastian ; Graf, Kathrin ; Dimmeler, Stefanie ; Hartung, Thomas ; Schumann, Ralf R. ; Hermann, Corinna. / Heterozygous toll-like receptor 4 polymorphism does not influence lipopolysaccharide-induced cytokine release in human whole blood. In: Journal of Infectious Diseases. 2003 ; Vol. 188, No. 6. pp. 938-943.
@article{7cc554093f2c419f859d73915201b394,
title = "Heterozygous toll-like receptor 4 polymorphism does not influence lipopolysaccharide-induced cytokine release in human whole blood",
abstract = "The heterozygous Asp299Gly mutation of the toll-like receptor (TLR) 4, the key receptor for lipopoiysaccharide (LPS), has been associated with attenuated inflammatory responses. When 160 healthy volunteers (9{\%} heterozygous and 0.6{\%} homozygous) were genotyped and their LPS-inducible cytokine release was assessed in an ex vivo whole blood test, the responses of heterozygotes did not differ significantly from those of wildtype carriers for any of the cytokines (tumor necrosis factor-α, interleukin [IL]-1β, IL-6, interferon-γ, and granulocyte colony-stimulating factor) or eicosanoids measured or for serum cytokines and C-reactive protein. Ten heterozygous subjects and 12 wild-type control subjects responded similarly to a graded series of LPS and Escherichia coli concentrations, excluding the possibility that allele-specific differences are evident only at low stimulus concentrations or in response to whole pathogens. These data demonstrate that the heterozygous Asp299Gly polymorphism does not exhibit a functional defect in cytokine release after the stimulation of blood monocytes.",
author = "{Von Aulock}, Sonja and Schr{\"o}der, {Nicolas W J} and Katja Gueinzius and Stephanie Traub and Sebastian Hoffmann and Kathrin Graf and Stefanie Dimmeler and Thomas Hartung and Schumann, {Ralf R.} and Corinna Hermann",
year = "2003",
month = "9",
day = "15",
doi = "10.1086/378095",
language = "English (US)",
volume = "188",
pages = "938--943",
journal = "Journal of Infectious Diseases",
issn = "0022-1899",
publisher = "Oxford University Press",
number = "6",

}

TY - JOUR

T1 - Heterozygous toll-like receptor 4 polymorphism does not influence lipopolysaccharide-induced cytokine release in human whole blood

AU - Von Aulock, Sonja

AU - Schröder, Nicolas W J

AU - Gueinzius, Katja

AU - Traub, Stephanie

AU - Hoffmann, Sebastian

AU - Graf, Kathrin

AU - Dimmeler, Stefanie

AU - Hartung, Thomas

AU - Schumann, Ralf R.

AU - Hermann, Corinna

PY - 2003/9/15

Y1 - 2003/9/15

N2 - The heterozygous Asp299Gly mutation of the toll-like receptor (TLR) 4, the key receptor for lipopoiysaccharide (LPS), has been associated with attenuated inflammatory responses. When 160 healthy volunteers (9% heterozygous and 0.6% homozygous) were genotyped and their LPS-inducible cytokine release was assessed in an ex vivo whole blood test, the responses of heterozygotes did not differ significantly from those of wildtype carriers for any of the cytokines (tumor necrosis factor-α, interleukin [IL]-1β, IL-6, interferon-γ, and granulocyte colony-stimulating factor) or eicosanoids measured or for serum cytokines and C-reactive protein. Ten heterozygous subjects and 12 wild-type control subjects responded similarly to a graded series of LPS and Escherichia coli concentrations, excluding the possibility that allele-specific differences are evident only at low stimulus concentrations or in response to whole pathogens. These data demonstrate that the heterozygous Asp299Gly polymorphism does not exhibit a functional defect in cytokine release after the stimulation of blood monocytes.

AB - The heterozygous Asp299Gly mutation of the toll-like receptor (TLR) 4, the key receptor for lipopoiysaccharide (LPS), has been associated with attenuated inflammatory responses. When 160 healthy volunteers (9% heterozygous and 0.6% homozygous) were genotyped and their LPS-inducible cytokine release was assessed in an ex vivo whole blood test, the responses of heterozygotes did not differ significantly from those of wildtype carriers for any of the cytokines (tumor necrosis factor-α, interleukin [IL]-1β, IL-6, interferon-γ, and granulocyte colony-stimulating factor) or eicosanoids measured or for serum cytokines and C-reactive protein. Ten heterozygous subjects and 12 wild-type control subjects responded similarly to a graded series of LPS and Escherichia coli concentrations, excluding the possibility that allele-specific differences are evident only at low stimulus concentrations or in response to whole pathogens. These data demonstrate that the heterozygous Asp299Gly polymorphism does not exhibit a functional defect in cytokine release after the stimulation of blood monocytes.

UR - http://www.scopus.com/inward/record.url?scp=0141840748&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0141840748&partnerID=8YFLogxK

U2 - 10.1086/378095

DO - 10.1086/378095

M3 - Article

VL - 188

SP - 938

EP - 943

JO - Journal of Infectious Diseases

JF - Journal of Infectious Diseases

SN - 0022-1899

IS - 6

ER -