Ventilator-induced lung injury is mediated by the NLRP3 inflammasome
The innate immune response is important in ventilator-induced lung injury (VILI) but the exact pathways involved are not elucidated. The authors studied the role of the intracellular danger sensor NLRP3 inflammasome. NLRP3 inflammasome gene expression was analyzed in respiratory epithelial cells and...
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| Vydáno v: | Anesthesiology (Philadelphia) Ročník 116; číslo 5; s. 1104 |
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01.05.2012
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| ISSN: | 1528-1175, 1528-1175 |
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| Abstract | The innate immune response is important in ventilator-induced lung injury (VILI) but the exact pathways involved are not elucidated. The authors studied the role of the intracellular danger sensor NLRP3 inflammasome.
NLRP3 inflammasome gene expression was analyzed in respiratory epithelial cells and alveolar macrophages obtained from ventilated patients (n = 40). In addition, wild-type and NLRP3 inflammasome deficient mice were randomized to low tidal volume (approximately 7.5 ml/kg) and high tidal volume (approximately 15 ml/kg) ventilation. The presence of uric acid in lung lavage, activation of caspase-1, and NLRP3 inflammasome gene expression in lung tissue were investigated. Moreover, mice were pretreated with interleukin-1 receptor antagonist, glibenclamide, or vehicle before start of mechanical ventilation. VILI endpoints were relative lung weights, total protein in lavage fluid, neutrophil influx, and pulmonary and systemic cytokine and chemokine concentrations. Data represent mean ± SD.
Mechanical ventilation up-regulated messenger RNA expression levels of NLRP3 in alveolar macrophages (1.0 ± 0 vs. 1.70 ± 1.65, P less than 0.05). In mice, mechanical ventilation increased both NLRP3 and apoptosis-associated speck-like protein messenger RNA levels, respectively (1.08 ± 0.55 vs. 3.98 ± 2.89; P less than 0.001 and 0.95 ± 0.53 vs. 6.0 ± 3.55; P less than 0.001), activated caspase-1, and increased uric acid levels (6.36 ± 1.85 vs. 41.9 ± 32.0, P less than 0.001). NLRP3 inflammasome deficient mice displayed less VILI due to high tidal volume mechanical ventilation compared with wild-type mice. Furthermore, treatment with interleukin-1 receptor antagonist or glibenclamide reduced VILI.
Mechanical ventilation induced a NLRP3 inflammasome dependent pulmonary inflammatory response. NLRP3 inflammasome deficiency partially protected mice from VILI. |
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| AbstractList | The innate immune response is important in ventilator-induced lung injury (VILI) but the exact pathways involved are not elucidated. The authors studied the role of the intracellular danger sensor NLRP3 inflammasome.
NLRP3 inflammasome gene expression was analyzed in respiratory epithelial cells and alveolar macrophages obtained from ventilated patients (n = 40). In addition, wild-type and NLRP3 inflammasome deficient mice were randomized to low tidal volume (approximately 7.5 ml/kg) and high tidal volume (approximately 15 ml/kg) ventilation. The presence of uric acid in lung lavage, activation of caspase-1, and NLRP3 inflammasome gene expression in lung tissue were investigated. Moreover, mice were pretreated with interleukin-1 receptor antagonist, glibenclamide, or vehicle before start of mechanical ventilation. VILI endpoints were relative lung weights, total protein in lavage fluid, neutrophil influx, and pulmonary and systemic cytokine and chemokine concentrations. Data represent mean ± SD.
Mechanical ventilation up-regulated messenger RNA expression levels of NLRP3 in alveolar macrophages (1.0 ± 0 vs. 1.70 ± 1.65, P less than 0.05). In mice, mechanical ventilation increased both NLRP3 and apoptosis-associated speck-like protein messenger RNA levels, respectively (1.08 ± 0.55 vs. 3.98 ± 2.89; P less than 0.001 and 0.95 ± 0.53 vs. 6.0 ± 3.55; P less than 0.001), activated caspase-1, and increased uric acid levels (6.36 ± 1.85 vs. 41.9 ± 32.0, P less than 0.001). NLRP3 inflammasome deficient mice displayed less VILI due to high tidal volume mechanical ventilation compared with wild-type mice. Furthermore, treatment with interleukin-1 receptor antagonist or glibenclamide reduced VILI.
Mechanical ventilation induced a NLRP3 inflammasome dependent pulmonary inflammatory response. NLRP3 inflammasome deficiency partially protected mice from VILI. The innate immune response is important in ventilator-induced lung injury (VILI) but the exact pathways involved are not elucidated. The authors studied the role of the intracellular danger sensor NLRP3 inflammasome.BACKGROUNDThe innate immune response is important in ventilator-induced lung injury (VILI) but the exact pathways involved are not elucidated. The authors studied the role of the intracellular danger sensor NLRP3 inflammasome.NLRP3 inflammasome gene expression was analyzed in respiratory epithelial cells and alveolar macrophages obtained from ventilated patients (n = 40). In addition, wild-type and NLRP3 inflammasome deficient mice were randomized to low tidal volume (approximately 7.5 ml/kg) and high tidal volume (approximately 15 ml/kg) ventilation. The presence of uric acid in lung lavage, activation of caspase-1, and NLRP3 inflammasome gene expression in lung tissue were investigated. Moreover, mice were pretreated with interleukin-1 receptor antagonist, glibenclamide, or vehicle before start of mechanical ventilation. VILI endpoints were relative lung weights, total protein in lavage fluid, neutrophil influx, and pulmonary and systemic cytokine and chemokine concentrations. Data represent mean ± SD.METHODSNLRP3 inflammasome gene expression was analyzed in respiratory epithelial cells and alveolar macrophages obtained from ventilated patients (n = 40). In addition, wild-type and NLRP3 inflammasome deficient mice were randomized to low tidal volume (approximately 7.5 ml/kg) and high tidal volume (approximately 15 ml/kg) ventilation. The presence of uric acid in lung lavage, activation of caspase-1, and NLRP3 inflammasome gene expression in lung tissue were investigated. Moreover, mice were pretreated with interleukin-1 receptor antagonist, glibenclamide, or vehicle before start of mechanical ventilation. VILI endpoints were relative lung weights, total protein in lavage fluid, neutrophil influx, and pulmonary and systemic cytokine and chemokine concentrations. Data represent mean ± SD.Mechanical ventilation up-regulated messenger RNA expression levels of NLRP3 in alveolar macrophages (1.0 ± 0 vs. 1.70 ± 1.65, P less than 0.05). In mice, mechanical ventilation increased both NLRP3 and apoptosis-associated speck-like protein messenger RNA levels, respectively (1.08 ± 0.55 vs. 3.98 ± 2.89; P less than 0.001 and 0.95 ± 0.53 vs. 6.0 ± 3.55; P less than 0.001), activated caspase-1, and increased uric acid levels (6.36 ± 1.85 vs. 41.9 ± 32.0, P less than 0.001). NLRP3 inflammasome deficient mice displayed less VILI due to high tidal volume mechanical ventilation compared with wild-type mice. Furthermore, treatment with interleukin-1 receptor antagonist or glibenclamide reduced VILI.RESULTSMechanical ventilation up-regulated messenger RNA expression levels of NLRP3 in alveolar macrophages (1.0 ± 0 vs. 1.70 ± 1.65, P less than 0.05). In mice, mechanical ventilation increased both NLRP3 and apoptosis-associated speck-like protein messenger RNA levels, respectively (1.08 ± 0.55 vs. 3.98 ± 2.89; P less than 0.001 and 0.95 ± 0.53 vs. 6.0 ± 3.55; P less than 0.001), activated caspase-1, and increased uric acid levels (6.36 ± 1.85 vs. 41.9 ± 32.0, P less than 0.001). NLRP3 inflammasome deficient mice displayed less VILI due to high tidal volume mechanical ventilation compared with wild-type mice. Furthermore, treatment with interleukin-1 receptor antagonist or glibenclamide reduced VILI.Mechanical ventilation induced a NLRP3 inflammasome dependent pulmonary inflammatory response. NLRP3 inflammasome deficiency partially protected mice from VILI.CONCLUSIONSMechanical ventilation induced a NLRP3 inflammasome dependent pulmonary inflammatory response. NLRP3 inflammasome deficiency partially protected mice from VILI. |
| Author | van der Sluijs, Koenraad F Leemans, Jaklien C Vlaar, Alexander P J Schultz, Marcus J Flavell, Richard A Choi, Goda Aslami, Hamid Wolthuis, Esther K Bresser, Paul Wieland, Catharina W Janczy, John R Sutterwala, Fayyaz S Roelofs, Joris J T H van der Poll, Tom Kuipers, Maria T |
| Author_xml | – sequence: 1 givenname: Maria T surname: Kuipers fullname: Kuipers, Maria T email: Ilse.Kuipers@amc.nl organization: Laboratory of Experimental Intensive Care and Anesthesiology (LEICA), and Center of Experimental and Molecular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. Ilse.Kuipers@amc.nl – sequence: 2 givenname: Hamid surname: Aslami fullname: Aslami, Hamid – sequence: 3 givenname: John R surname: Janczy fullname: Janczy, John R – sequence: 4 givenname: Koenraad F surname: van der Sluijs fullname: van der Sluijs, Koenraad F – sequence: 5 givenname: Alexander P J surname: Vlaar fullname: Vlaar, Alexander P J – sequence: 6 givenname: Esther K surname: Wolthuis fullname: Wolthuis, Esther K – sequence: 7 givenname: Goda surname: Choi fullname: Choi, Goda – sequence: 8 givenname: Joris J T H surname: Roelofs fullname: Roelofs, Joris J T H – sequence: 9 givenname: Richard A surname: Flavell fullname: Flavell, Richard A – sequence: 10 givenname: Fayyaz S surname: Sutterwala fullname: Sutterwala, Fayyaz S – sequence: 11 givenname: Paul surname: Bresser fullname: Bresser, Paul – sequence: 12 givenname: Jaklien C surname: Leemans fullname: Leemans, Jaklien C – sequence: 13 givenname: Tom surname: van der Poll fullname: van der Poll, Tom – sequence: 14 givenname: Marcus J surname: Schultz fullname: Schultz, Marcus J – sequence: 15 givenname: Catharina W surname: Wieland fullname: Wieland, Catharina W |
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| Snippet | The innate immune response is important in ventilator-induced lung injury (VILI) but the exact pathways involved are not elucidated. The authors studied the... |
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| SubjectTerms | Animals Bronchoalveolar Lavage Fluid - chemistry Carrier Proteins - genetics Carrier Proteins - physiology Caspase 1 - metabolism Cytokines - blood Cytokines - metabolism Enzyme Activation - physiology Epithelial Cells - metabolism Glyburide - pharmacology Humans Inflammasomes - genetics Macrophages, Alveolar - metabolism Mice Mice, Inbred C57BL Mice, Knockout Neutrophil Infiltration NLR Family, Pyrin Domain-Containing 3 Protein Organ Size - physiology Receptors, Interleukin-1 - antagonists & inhibitors Respiration, Artificial RNA, Messenger - biosynthesis RNA, Messenger - genetics Tidal Volume - physiology Up-Regulation - physiology Uric Acid - metabolism Ventilator-Induced Lung Injury - genetics Ventilator-Induced Lung Injury - pathology |
| Title | Ventilator-induced lung injury is mediated by the NLRP3 inflammasome |
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