Publication

TLR2 deficiency aggravates lung injury caused by mechanical ventilation

Kuipers, M. T., Jongsma, G., Hegeman, M. A., Tuip-de Boer, A. M., Wolthuis, E. K., Choi, G., Bresser, P., van der Poll, T., Schultz, M. J. & Wieland, C. W., Jul-2014, In : Shock. 42, 1, p. 60-64 5 p.

Research output: Contribution to journalArticleAcademicpeer-review

APA

Kuipers, M. T., Jongsma, G., Hegeman, M. A., Tuip-de Boer, A. M., Wolthuis, E. K., Choi, G., ... Wieland, C. W. (2014). TLR2 deficiency aggravates lung injury caused by mechanical ventilation. Shock, 42(1), 60-64. https://doi.org/10.1097/SHK.0000000000000172

Author

Kuipers, Maria Theresa ; Jongsma, Geartsje ; Hegeman, Maria A ; Tuip-de Boer, Anita M ; Wolthuis, Esther K ; Choi, Goda ; Bresser, Paul ; van der Poll, Tom ; Schultz, Marcus J ; Wieland, Catharina W. / TLR2 deficiency aggravates lung injury caused by mechanical ventilation. In: Shock. 2014 ; Vol. 42, No. 1. pp. 60-64.

Harvard

Kuipers, MT, Jongsma, G, Hegeman, MA, Tuip-de Boer, AM, Wolthuis, EK, Choi, G, Bresser, P, van der Poll, T, Schultz, MJ & Wieland, CW 2014, 'TLR2 deficiency aggravates lung injury caused by mechanical ventilation', Shock, vol. 42, no. 1, pp. 60-64. https://doi.org/10.1097/SHK.0000000000000172

Standard

TLR2 deficiency aggravates lung injury caused by mechanical ventilation. / Kuipers, Maria Theresa; Jongsma, Geartsje; Hegeman, Maria A; Tuip-de Boer, Anita M; Wolthuis, Esther K; Choi, Goda; Bresser, Paul; van der Poll, Tom; Schultz, Marcus J; Wieland, Catharina W.

In: Shock, Vol. 42, No. 1, 07.2014, p. 60-64.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

Kuipers MT, Jongsma G, Hegeman MA, Tuip-de Boer AM, Wolthuis EK, Choi G et al. TLR2 deficiency aggravates lung injury caused by mechanical ventilation. Shock. 2014 Jul;42(1):60-64. https://doi.org/10.1097/SHK.0000000000000172


BibTeX

@article{2f77b1ca8f6b48998e1c969670870ef2,
title = "TLR2 deficiency aggravates lung injury caused by mechanical ventilation",
abstract = "Innate immunity pathways are found to play an important role in ventilator-induced lung injury. We analyzed pulmonary expression of Toll-like receptor 2 (TLR2) in humans and mice and determined the role of TLR2 in the pathogenesis of ventilator-induced lung injury in mice. Toll-like receptor 2 gene expression was analyzed in human bronchoalveolar lavage fluid (BALF) cells and murine lung tissue after 5 h of ventilation. In addition, wild-type (WT) and TLR2 knockout (KO) mice were ventilated with either lower tidal volumes (VT) of 7 mL/kg with positive end-expiratory pressure (PEEP) or higher VT of 15 mL/kg without PEEP for 5 h. Spontaneously breathing mice served as controls. Total protein and immunoglobulin M levels in BALF, neutrophil influx into the alveolar compartment, and interleukin 6 (IL-6), IL-1β, and keratinocyte-derived chemokine concentrations in lung tissue homogenates were measured. We observed enhanced TLR2 gene expression in BALF cells of ventilated patients and in lung tissue of ventilated mice. In WT mice, ventilation with higher VT without PEEP resulted in lung injury and inflammation with higher immunoglobulin M levels, neutrophil influx, and levels of inflammatory mediators compared with controls. In TLR2 KO mice, neutrophil influx and IL-6, IL-1β, and keratinocyte-derived chemokine were enhanced by this ventilation strategy. Ventilation with lower VT with PEEP only increased neutrophil influx and was similar in WT and TLR2 KO mice. In summary, injurious ventilation enhances TLR2 expression in lungs. Toll-like receptor 2 deficiency does not protect lungs from ventilator-induced lung injury. In contrast, ventilation with higher VT without PEEP aggravates inflammation in TLR2 KO mice.",
keywords = "Animals, Bronchoalveolar Lavage Fluid, Carbon Dioxide, Gene Expression Regulation, Humans, Lung, Mice, Inbred C57BL, Mice, Knockout, Oxygen, Partial Pressure, Positive-Pressure Respiration, RNA, Messenger, Respiration, Artificial, Toll-Like Receptor 2, Ventilator-Induced Lung Injury",
author = "Kuipers, {Maria Theresa} and Geartsje Jongsma and Hegeman, {Maria A} and {Tuip-de Boer}, {Anita M} and Wolthuis, {Esther K} and Goda Choi and Paul Bresser and {van der Poll}, Tom and Schultz, {Marcus J} and Wieland, {Catharina W}",
year = "2014",
month = "7",
doi = "10.1097/SHK.0000000000000172",
language = "English",
volume = "42",
pages = "60--64",
journal = "Shock",
issn = "1073-2322",
publisher = "LIPPINCOTT WILLIAMS & WILKINS",
number = "1",

}

RIS

TY - JOUR

T1 - TLR2 deficiency aggravates lung injury caused by mechanical ventilation

AU - Kuipers, Maria Theresa

AU - Jongsma, Geartsje

AU - Hegeman, Maria A

AU - Tuip-de Boer, Anita M

AU - Wolthuis, Esther K

AU - Choi, Goda

AU - Bresser, Paul

AU - van der Poll, Tom

AU - Schultz, Marcus J

AU - Wieland, Catharina W

PY - 2014/7

Y1 - 2014/7

N2 - Innate immunity pathways are found to play an important role in ventilator-induced lung injury. We analyzed pulmonary expression of Toll-like receptor 2 (TLR2) in humans and mice and determined the role of TLR2 in the pathogenesis of ventilator-induced lung injury in mice. Toll-like receptor 2 gene expression was analyzed in human bronchoalveolar lavage fluid (BALF) cells and murine lung tissue after 5 h of ventilation. In addition, wild-type (WT) and TLR2 knockout (KO) mice were ventilated with either lower tidal volumes (VT) of 7 mL/kg with positive end-expiratory pressure (PEEP) or higher VT of 15 mL/kg without PEEP for 5 h. Spontaneously breathing mice served as controls. Total protein and immunoglobulin M levels in BALF, neutrophil influx into the alveolar compartment, and interleukin 6 (IL-6), IL-1β, and keratinocyte-derived chemokine concentrations in lung tissue homogenates were measured. We observed enhanced TLR2 gene expression in BALF cells of ventilated patients and in lung tissue of ventilated mice. In WT mice, ventilation with higher VT without PEEP resulted in lung injury and inflammation with higher immunoglobulin M levels, neutrophil influx, and levels of inflammatory mediators compared with controls. In TLR2 KO mice, neutrophil influx and IL-6, IL-1β, and keratinocyte-derived chemokine were enhanced by this ventilation strategy. Ventilation with lower VT with PEEP only increased neutrophil influx and was similar in WT and TLR2 KO mice. In summary, injurious ventilation enhances TLR2 expression in lungs. Toll-like receptor 2 deficiency does not protect lungs from ventilator-induced lung injury. In contrast, ventilation with higher VT without PEEP aggravates inflammation in TLR2 KO mice.

AB - Innate immunity pathways are found to play an important role in ventilator-induced lung injury. We analyzed pulmonary expression of Toll-like receptor 2 (TLR2) in humans and mice and determined the role of TLR2 in the pathogenesis of ventilator-induced lung injury in mice. Toll-like receptor 2 gene expression was analyzed in human bronchoalveolar lavage fluid (BALF) cells and murine lung tissue after 5 h of ventilation. In addition, wild-type (WT) and TLR2 knockout (KO) mice were ventilated with either lower tidal volumes (VT) of 7 mL/kg with positive end-expiratory pressure (PEEP) or higher VT of 15 mL/kg without PEEP for 5 h. Spontaneously breathing mice served as controls. Total protein and immunoglobulin M levels in BALF, neutrophil influx into the alveolar compartment, and interleukin 6 (IL-6), IL-1β, and keratinocyte-derived chemokine concentrations in lung tissue homogenates were measured. We observed enhanced TLR2 gene expression in BALF cells of ventilated patients and in lung tissue of ventilated mice. In WT mice, ventilation with higher VT without PEEP resulted in lung injury and inflammation with higher immunoglobulin M levels, neutrophil influx, and levels of inflammatory mediators compared with controls. In TLR2 KO mice, neutrophil influx and IL-6, IL-1β, and keratinocyte-derived chemokine were enhanced by this ventilation strategy. Ventilation with lower VT with PEEP only increased neutrophil influx and was similar in WT and TLR2 KO mice. In summary, injurious ventilation enhances TLR2 expression in lungs. Toll-like receptor 2 deficiency does not protect lungs from ventilator-induced lung injury. In contrast, ventilation with higher VT without PEEP aggravates inflammation in TLR2 KO mice.

KW - Animals

KW - Bronchoalveolar Lavage Fluid

KW - Carbon Dioxide

KW - Gene Expression Regulation

KW - Humans

KW - Lung

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Oxygen

KW - Partial Pressure

KW - Positive-Pressure Respiration

KW - RNA, Messenger

KW - Respiration, Artificial

KW - Toll-Like Receptor 2

KW - Ventilator-Induced Lung Injury

U2 - 10.1097/SHK.0000000000000172

DO - 10.1097/SHK.0000000000000172

M3 - Article

C2 - 24667617

VL - 42

SP - 60

EP - 64

JO - Shock

JF - Shock

SN - 1073-2322

IS - 1

ER -

ID: 29060765