Publication

Endotoxin increases plasma soluble tumor necrosis factor-related apoptosis-inducing ligand level mediated by the p38 mitogen-activated protein kinase signaling pathway

Lub-de Hooge, M. N., de Jong, S., Vermot-Desroches, C., Tulleken, J. E., de Vries, E. G. E. & Zijlstra, J. G., 2004, In : Shock. 22, 2, p. 186 - 188 3 p.

Research output: Contribution to journalArticleAcademicpeer-review

APA

Lub-de Hooge, M. N., de Jong, S., Vermot-Desroches, C., Tulleken, J. E., de Vries, E. G. E., & Zijlstra, J. G. (2004). Endotoxin increases plasma soluble tumor necrosis factor-related apoptosis-inducing ligand level mediated by the p38 mitogen-activated protein kinase signaling pathway. Shock, 22(2), 186 - 188. https://doi.org/10.1097/01.shk.0000132489.82177.ec

Author

Lub-de Hooge, Marjolin N ; de Jong, Steven ; Vermot-Desroches, Claudine ; Tulleken, Jaap E ; de Vries, Elisabeth G E ; Zijlstra, Jan G. / Endotoxin increases plasma soluble tumor necrosis factor-related apoptosis-inducing ligand level mediated by the p38 mitogen-activated protein kinase signaling pathway. In: Shock. 2004 ; Vol. 22, No. 2. pp. 186 - 188.

Harvard

Lub-de Hooge, MN, de Jong, S, Vermot-Desroches, C, Tulleken, JE, de Vries, EGE & Zijlstra, JG 2004, 'Endotoxin increases plasma soluble tumor necrosis factor-related apoptosis-inducing ligand level mediated by the p38 mitogen-activated protein kinase signaling pathway', Shock, vol. 22, no. 2, pp. 186 - 188. https://doi.org/10.1097/01.shk.0000132489.82177.ec

Standard

Endotoxin increases plasma soluble tumor necrosis factor-related apoptosis-inducing ligand level mediated by the p38 mitogen-activated protein kinase signaling pathway. / Lub-de Hooge, Marjolin N; de Jong, Steven; Vermot-Desroches, Claudine; Tulleken, Jaap E; de Vries, Elisabeth G E; Zijlstra, Jan G.

In: Shock, Vol. 22, No. 2, 2004, p. 186 - 188.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

Lub-de Hooge MN, de Jong S, Vermot-Desroches C, Tulleken JE, de Vries EGE, Zijlstra JG. Endotoxin increases plasma soluble tumor necrosis factor-related apoptosis-inducing ligand level mediated by the p38 mitogen-activated protein kinase signaling pathway. Shock. 2004;22(2):186 - 188. https://doi.org/10.1097/01.shk.0000132489.82177.ec


BibTeX

@article{ba17945c15554eb8801e8ca4240a2713,
title = "Endotoxin increases plasma soluble tumor necrosis factor-related apoptosis-inducing ligand level mediated by the p38 mitogen-activated protein kinase signaling pathway",
abstract = "Despite extensive knowledge about the mechanisms behind sepsis, this syndrome still caries a large morbidity and mortality rate. Dysregulated immune and coagulation systems are held responsible. However, additional pathophysiological mechanisms such as uncontrolled apoptosis induced by death receptor ligands might well play a role. P38 mitogen-activated protein (MAP) kinase inhibitors are considered as potential drugs in inflammatory diseases. Therefore, the effect of endotoxin administration on the response of soluble(s) tumor necrosis factor-related apoptosis-inducing ligand (sTRAIL), a death receptor ligand, and the role of p38 MAP kinase inhibition was studied in 21 human volunteers. The volunteers received 30 min before the endotoxin infusion a single oral dose of placebo or the selective p38 MAP kinase inhibitor drug, RWJ-67657. Plasma sTRAIL increased 10-fold to 6564 +/- 511 pg/mL after 2.5 h. This increase was blocked completely by the highest dose of RW-J6765. This is the first report showing that endotoxin increases sTRAIL where the p38 MAP kinase signaling pathway is involved.",
keywords = "endotoxemia, sepsis, TRAIL, apoptosis, p38 MAPK, SEVERE SEPSIS, CYTOKINE PRODUCTION, SEPTIC SHOCK, MAP-KINASE, FAMILY, NEUTROPHILS, SUPPRESSION, INHIBITION, EXPRESSION, CHALLENGE",
author = "{Lub-de Hooge}, {Marjolin N} and {de Jong}, Steven and Claudine Vermot-Desroches and Tulleken, {Jaap E} and {de Vries}, {Elisabeth G E} and Zijlstra, {Jan G}",
note = "Article",
year = "2004",
doi = "10.1097/01.shk.0000132489.82177.ec",
language = "English",
volume = "22",
pages = "186 -- 188",
journal = "Shock",
issn = "1073-2322",
publisher = "LIPPINCOTT WILLIAMS & WILKINS",
number = "2",

}

RIS

TY - JOUR

T1 - Endotoxin increases plasma soluble tumor necrosis factor-related apoptosis-inducing ligand level mediated by the p38 mitogen-activated protein kinase signaling pathway

AU - Lub-de Hooge, Marjolin N

AU - de Jong, Steven

AU - Vermot-Desroches, Claudine

AU - Tulleken, Jaap E

AU - de Vries, Elisabeth G E

AU - Zijlstra, Jan G

N1 - Article

PY - 2004

Y1 - 2004

N2 - Despite extensive knowledge about the mechanisms behind sepsis, this syndrome still caries a large morbidity and mortality rate. Dysregulated immune and coagulation systems are held responsible. However, additional pathophysiological mechanisms such as uncontrolled apoptosis induced by death receptor ligands might well play a role. P38 mitogen-activated protein (MAP) kinase inhibitors are considered as potential drugs in inflammatory diseases. Therefore, the effect of endotoxin administration on the response of soluble(s) tumor necrosis factor-related apoptosis-inducing ligand (sTRAIL), a death receptor ligand, and the role of p38 MAP kinase inhibition was studied in 21 human volunteers. The volunteers received 30 min before the endotoxin infusion a single oral dose of placebo or the selective p38 MAP kinase inhibitor drug, RWJ-67657. Plasma sTRAIL increased 10-fold to 6564 +/- 511 pg/mL after 2.5 h. This increase was blocked completely by the highest dose of RW-J6765. This is the first report showing that endotoxin increases sTRAIL where the p38 MAP kinase signaling pathway is involved.

AB - Despite extensive knowledge about the mechanisms behind sepsis, this syndrome still caries a large morbidity and mortality rate. Dysregulated immune and coagulation systems are held responsible. However, additional pathophysiological mechanisms such as uncontrolled apoptosis induced by death receptor ligands might well play a role. P38 mitogen-activated protein (MAP) kinase inhibitors are considered as potential drugs in inflammatory diseases. Therefore, the effect of endotoxin administration on the response of soluble(s) tumor necrosis factor-related apoptosis-inducing ligand (sTRAIL), a death receptor ligand, and the role of p38 MAP kinase inhibition was studied in 21 human volunteers. The volunteers received 30 min before the endotoxin infusion a single oral dose of placebo or the selective p38 MAP kinase inhibitor drug, RWJ-67657. Plasma sTRAIL increased 10-fold to 6564 +/- 511 pg/mL after 2.5 h. This increase was blocked completely by the highest dose of RW-J6765. This is the first report showing that endotoxin increases sTRAIL where the p38 MAP kinase signaling pathway is involved.

KW - endotoxemia

KW - sepsis

KW - TRAIL

KW - apoptosis

KW - p38 MAPK

KW - SEVERE SEPSIS

KW - CYTOKINE PRODUCTION

KW - SEPTIC SHOCK

KW - MAP-KINASE

KW - FAMILY

KW - NEUTROPHILS

KW - SUPPRESSION

KW - INHIBITION

KW - EXPRESSION

KW - CHALLENGE

U2 - 10.1097/01.shk.0000132489.82177.ec

DO - 10.1097/01.shk.0000132489.82177.ec

M3 - Article

VL - 22

SP - 186

EP - 188

JO - Shock

JF - Shock

SN - 1073-2322

IS - 2

ER -

ID: 1556578