Effect of antibody-mediated connective tissue growth factor neutralization on lung edema in ventilator-induced lung injury in rats
Background Acute respiratory distress syndrome (ARDS) is characterized by alveolar edema that can progress to septal fibrosis. Mechanical ventilation can augment lung injury, termed ventilator-induced lung injury (VILI). Connective tissue growth factor (CTGF), a mediator of fibrosis, is increased in...
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| Vydáno v: | Molecular medicine (Cambridge, Mass.) Ročník 30; číslo 1; s. 68 - 11 |
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| Hlavní autoři: | , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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London
BioMed Central
22.05.2024
Springer Nature B.V BMC |
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| ISSN: | 1528-3658, 1076-1551, 1528-3658 |
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| Abstract | Background
Acute respiratory distress syndrome (ARDS) is characterized by alveolar edema that can progress to septal fibrosis. Mechanical ventilation can augment lung injury, termed ventilator-induced lung injury (VILI). Connective tissue growth factor (CTGF), a mediator of fibrosis, is increased in ARDS patients. Blocking CTGF inhibits fibrosis and possibly vascular leakage. This study investigated whether neutralizing CTGF reduces pulmonary edema in VILI.
Methods
Following LPS administration, rats were mechanically ventilated for 6 h with low (6 mL/kg; low V
T
) or moderate (10 mL/kg; mod V
T
) tidal volume and treated with a neutralizing CTGF antibody (FG-3154) or placebo lgG (vehicle). Control rats without LPS were ventilated for 6 h with low V
T
. Lung wet-to-dry weight ratio, FITC-labeled dextran permeability, histopathology, and soluble RAGE were determined.
Results
VILI was characterized by reduced PaO
2
/FiO
2
ratio (low V
T
: 540 [381–661] vs. control: 693 [620–754], p < 0.05), increased wet-to-dry weight ratio (low V
T
: 4.8 [4.6–4.9] vs. control: 4.5 [4.4–4.6], p < 0.05), pneumonia (low V
T
: 30 [0–58] vs. control: 0 [0–0]%, p < 0.05) and interstitial inflammation (low V
T
: 2 [1–3] vs. control: 1 [0–1], p < 0.05). FG-3154 did not affect wet-to-dry weight ratio (mod V
T
+ FG-3154: 4.8 [4.7–5.0] vs. mod V
T
+ vehicle: 4.8 [4.8–5.0], p > 0.99), extravasated dextrans (mod V
T
+ FG-3154: 0.06 [0.04–0.09] vs. mod V
T
+ vehicle: 0.04 [0.03–0.09] µg/mg tissue, p > 0.99), sRAGE (mod V
T
+ FG-3154: 1865 [1628–2252] vs. mod V
T
+ vehicle: 1885 [1695–2159] pg/mL, p > 0.99) or histopathology.
Conclusions
‘Double hit’ VILI was characterized by inflammation, impaired oxygenation, pulmonary edema and histopathological lung injury. Blocking CTGF does not improve oxygenation nor reduce pulmonary edema in rats with VILI.
Graphical Abstract |
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| AbstractList | Acute respiratory distress syndrome (ARDS) is characterized by alveolar edema that can progress to septal fibrosis. Mechanical ventilation can augment lung injury, termed ventilator-induced lung injury (VILI). Connective tissue growth factor (CTGF), a mediator of fibrosis, is increased in ARDS patients. Blocking CTGF inhibits fibrosis and possibly vascular leakage. This study investigated whether neutralizing CTGF reduces pulmonary edema in VILI.BACKGROUNDAcute respiratory distress syndrome (ARDS) is characterized by alveolar edema that can progress to septal fibrosis. Mechanical ventilation can augment lung injury, termed ventilator-induced lung injury (VILI). Connective tissue growth factor (CTGF), a mediator of fibrosis, is increased in ARDS patients. Blocking CTGF inhibits fibrosis and possibly vascular leakage. This study investigated whether neutralizing CTGF reduces pulmonary edema in VILI.Following LPS administration, rats were mechanically ventilated for 6 h with low (6 mL/kg; low VT) or moderate (10 mL/kg; mod VT) tidal volume and treated with a neutralizing CTGF antibody (FG-3154) or placebo lgG (vehicle). Control rats without LPS were ventilated for 6 h with low VT. Lung wet-to-dry weight ratio, FITC-labeled dextran permeability, histopathology, and soluble RAGE were determined.METHODSFollowing LPS administration, rats were mechanically ventilated for 6 h with low (6 mL/kg; low VT) or moderate (10 mL/kg; mod VT) tidal volume and treated with a neutralizing CTGF antibody (FG-3154) or placebo lgG (vehicle). Control rats without LPS were ventilated for 6 h with low VT. Lung wet-to-dry weight ratio, FITC-labeled dextran permeability, histopathology, and soluble RAGE were determined.VILI was characterized by reduced PaO2/FiO2 ratio (low VT: 540 [381-661] vs. control: 693 [620-754], p < 0.05), increased wet-to-dry weight ratio (low VT: 4.8 [4.6-4.9] vs. control: 4.5 [4.4-4.6], p < 0.05), pneumonia (low VT: 30 [0-58] vs. control: 0 [0-0]%, p < 0.05) and interstitial inflammation (low VT: 2 [1-3] vs. control: 1 [0-1], p < 0.05). FG-3154 did not affect wet-to-dry weight ratio (mod VT + FG-3154: 4.8 [4.7-5.0] vs. mod VT + vehicle: 4.8 [4.8-5.0], p > 0.99), extravasated dextrans (mod VT + FG-3154: 0.06 [0.04-0.09] vs. mod VT + vehicle: 0.04 [0.03-0.09] µg/mg tissue, p > 0.99), sRAGE (mod VT + FG-3154: 1865 [1628-2252] vs. mod VT + vehicle: 1885 [1695-2159] pg/mL, p > 0.99) or histopathology.RESULTSVILI was characterized by reduced PaO2/FiO2 ratio (low VT: 540 [381-661] vs. control: 693 [620-754], p < 0.05), increased wet-to-dry weight ratio (low VT: 4.8 [4.6-4.9] vs. control: 4.5 [4.4-4.6], p < 0.05), pneumonia (low VT: 30 [0-58] vs. control: 0 [0-0]%, p < 0.05) and interstitial inflammation (low VT: 2 [1-3] vs. control: 1 [0-1], p < 0.05). FG-3154 did not affect wet-to-dry weight ratio (mod VT + FG-3154: 4.8 [4.7-5.0] vs. mod VT + vehicle: 4.8 [4.8-5.0], p > 0.99), extravasated dextrans (mod VT + FG-3154: 0.06 [0.04-0.09] vs. mod VT + vehicle: 0.04 [0.03-0.09] µg/mg tissue, p > 0.99), sRAGE (mod VT + FG-3154: 1865 [1628-2252] vs. mod VT + vehicle: 1885 [1695-2159] pg/mL, p > 0.99) or histopathology.'Double hit' VILI was characterized by inflammation, impaired oxygenation, pulmonary edema and histopathological lung injury. Blocking CTGF does not improve oxygenation nor reduce pulmonary edema in rats with VILI.CONCLUSIONS'Double hit' VILI was characterized by inflammation, impaired oxygenation, pulmonary edema and histopathological lung injury. Blocking CTGF does not improve oxygenation nor reduce pulmonary edema in rats with VILI. BackgroundAcute respiratory distress syndrome (ARDS) is characterized by alveolar edema that can progress to septal fibrosis. Mechanical ventilation can augment lung injury, termed ventilator-induced lung injury (VILI). Connective tissue growth factor (CTGF), a mediator of fibrosis, is increased in ARDS patients. Blocking CTGF inhibits fibrosis and possibly vascular leakage. This study investigated whether neutralizing CTGF reduces pulmonary edema in VILI.MethodsFollowing LPS administration, rats were mechanically ventilated for 6 h with low (6 mL/kg; low VT) or moderate (10 mL/kg; mod VT) tidal volume and treated with a neutralizing CTGF antibody (FG-3154) or placebo lgG (vehicle). Control rats without LPS were ventilated for 6 h with low VT. Lung wet-to-dry weight ratio, FITC-labeled dextran permeability, histopathology, and soluble RAGE were determined.ResultsVILI was characterized by reduced PaO2/FiO2 ratio (low VT: 540 [381–661] vs. control: 693 [620–754], p < 0.05), increased wet-to-dry weight ratio (low VT: 4.8 [4.6–4.9] vs. control: 4.5 [4.4–4.6], p < 0.05), pneumonia (low VT: 30 [0–58] vs. control: 0 [0–0]%, p < 0.05) and interstitial inflammation (low VT: 2 [1–3] vs. control: 1 [0–1], p < 0.05). FG-3154 did not affect wet-to-dry weight ratio (mod VT + FG-3154: 4.8 [4.7–5.0] vs. mod VT + vehicle: 4.8 [4.8–5.0], p > 0.99), extravasated dextrans (mod VT + FG-3154: 0.06 [0.04–0.09] vs. mod VT + vehicle: 0.04 [0.03–0.09] µg/mg tissue, p > 0.99), sRAGE (mod VT + FG-3154: 1865 [1628–2252] vs. mod VT + vehicle: 1885 [1695–2159] pg/mL, p > 0.99) or histopathology.Conclusions‘Double hit’ VILI was characterized by inflammation, impaired oxygenation, pulmonary edema and histopathological lung injury. Blocking CTGF does not improve oxygenation nor reduce pulmonary edema in rats with VILI. Abstract Background Acute respiratory distress syndrome (ARDS) is characterized by alveolar edema that can progress to septal fibrosis. Mechanical ventilation can augment lung injury, termed ventilator-induced lung injury (VILI). Connective tissue growth factor (CTGF), a mediator of fibrosis, is increased in ARDS patients. Blocking CTGF inhibits fibrosis and possibly vascular leakage. This study investigated whether neutralizing CTGF reduces pulmonary edema in VILI. Methods Following LPS administration, rats were mechanically ventilated for 6 h with low (6 mL/kg; low VT) or moderate (10 mL/kg; mod VT) tidal volume and treated with a neutralizing CTGF antibody (FG-3154) or placebo lgG (vehicle). Control rats without LPS were ventilated for 6 h with low VT. Lung wet-to-dry weight ratio, FITC-labeled dextran permeability, histopathology, and soluble RAGE were determined. Results VILI was characterized by reduced PaO2/FiO2 ratio (low VT: 540 [381–661] vs. control: 693 [620–754], p < 0.05), increased wet-to-dry weight ratio (low VT: 4.8 [4.6–4.9] vs. control: 4.5 [4.4–4.6], p < 0.05), pneumonia (low VT: 30 [0–58] vs. control: 0 [0–0]%, p < 0.05) and interstitial inflammation (low VT: 2 [1–3] vs. control: 1 [0–1], p < 0.05). FG-3154 did not affect wet-to-dry weight ratio (mod VT + FG-3154: 4.8 [4.7–5.0] vs. mod VT + vehicle: 4.8 [4.8–5.0], p > 0.99), extravasated dextrans (mod VT + FG-3154: 0.06 [0.04–0.09] vs. mod VT + vehicle: 0.04 [0.03–0.09] µg/mg tissue, p > 0.99), sRAGE (mod VT + FG-3154: 1865 [1628–2252] vs. mod VT + vehicle: 1885 [1695–2159] pg/mL, p > 0.99) or histopathology. Conclusions ‘Double hit’ VILI was characterized by inflammation, impaired oxygenation, pulmonary edema and histopathological lung injury. Blocking CTGF does not improve oxygenation nor reduce pulmonary edema in rats with VILI. Graphical Abstract Background Acute respiratory distress syndrome (ARDS) is characterized by alveolar edema that can progress to septal fibrosis. Mechanical ventilation can augment lung injury, termed ventilator-induced lung injury (VILI). Connective tissue growth factor (CTGF), a mediator of fibrosis, is increased in ARDS patients. Blocking CTGF inhibits fibrosis and possibly vascular leakage. This study investigated whether neutralizing CTGF reduces pulmonary edema in VILI. Methods Following LPS administration, rats were mechanically ventilated for 6 h with low (6 mL/kg; low V T ) or moderate (10 mL/kg; mod V T ) tidal volume and treated with a neutralizing CTGF antibody (FG-3154) or placebo lgG (vehicle). Control rats without LPS were ventilated for 6 h with low V T . Lung wet-to-dry weight ratio, FITC-labeled dextran permeability, histopathology, and soluble RAGE were determined. Results VILI was characterized by reduced PaO 2 /FiO 2 ratio (low V T : 540 [381–661] vs. control: 693 [620–754], p < 0.05), increased wet-to-dry weight ratio (low V T : 4.8 [4.6–4.9] vs. control: 4.5 [4.4–4.6], p < 0.05), pneumonia (low V T : 30 [0–58] vs. control: 0 [0–0]%, p < 0.05) and interstitial inflammation (low V T : 2 [1–3] vs. control: 1 [0–1], p < 0.05). FG-3154 did not affect wet-to-dry weight ratio (mod V T + FG-3154: 4.8 [4.7–5.0] vs. mod V T + vehicle: 4.8 [4.8–5.0], p > 0.99), extravasated dextrans (mod V T + FG-3154: 0.06 [0.04–0.09] vs. mod V T + vehicle: 0.04 [0.03–0.09] µg/mg tissue, p > 0.99), sRAGE (mod V T + FG-3154: 1865 [1628–2252] vs. mod V T + vehicle: 1885 [1695–2159] pg/mL, p > 0.99) or histopathology. Conclusions ‘Double hit’ VILI was characterized by inflammation, impaired oxygenation, pulmonary edema and histopathological lung injury. Blocking CTGF does not improve oxygenation nor reduce pulmonary edema in rats with VILI. Graphical Abstract Acute respiratory distress syndrome (ARDS) is characterized by alveolar edema that can progress to septal fibrosis. Mechanical ventilation can augment lung injury, termed ventilator-induced lung injury (VILI). Connective tissue growth factor (CTGF), a mediator of fibrosis, is increased in ARDS patients. Blocking CTGF inhibits fibrosis and possibly vascular leakage. This study investigated whether neutralizing CTGF reduces pulmonary edema in VILI. Following LPS administration, rats were mechanically ventilated for 6 h with low (6 mL/kg; low V ) or moderate (10 mL/kg; mod V ) tidal volume and treated with a neutralizing CTGF antibody (FG-3154) or placebo lgG (vehicle). Control rats without LPS were ventilated for 6 h with low V . Lung wet-to-dry weight ratio, FITC-labeled dextran permeability, histopathology, and soluble RAGE were determined. VILI was characterized by reduced PaO /FiO ratio (low V : 540 [381-661] vs. control: 693 [620-754], p < 0.05), increased wet-to-dry weight ratio (low V : 4.8 [4.6-4.9] vs. control: 4.5 [4.4-4.6], p < 0.05), pneumonia (low V : 30 [0-58] vs. control: 0 [0-0]%, p < 0.05) and interstitial inflammation (low V : 2 [1-3] vs. control: 1 [0-1], p < 0.05). FG-3154 did not affect wet-to-dry weight ratio (mod V + FG-3154: 4.8 [4.7-5.0] vs. mod V + vehicle: 4.8 [4.8-5.0], p > 0.99), extravasated dextrans (mod V + FG-3154: 0.06 [0.04-0.09] vs. mod V + vehicle: 0.04 [0.03-0.09] µg/mg tissue, p > 0.99), sRAGE (mod V + FG-3154: 1865 [1628-2252] vs. mod V + vehicle: 1885 [1695-2159] pg/mL, p > 0.99) or histopathology. 'Double hit' VILI was characterized by inflammation, impaired oxygenation, pulmonary edema and histopathological lung injury. Blocking CTGF does not improve oxygenation nor reduce pulmonary edema in rats with VILI. |
| ArticleNumber | 68 |
| Author | Ibelings, Roselique van den Brom, Charissa E. Polet, Chantal A. Bozic, Caitlin Roelofs, Joris J. T. H. Juffermans, Nicole P. Bongers, Annabel Tuip-de Boer, Anita M. |
| Author_xml | – sequence: 1 givenname: Charissa E. orcidid: 0000-0002-0886-1388 surname: van den Brom fullname: van den Brom, Charissa E. email: c.vandenbrom@amsterdamumc.nl organization: Department of Anesthesiology, Amsterdam UMC, VU University, Laboratory for Experimental Intensive Care and Anesthesiology (LEICA), Amsterdam UMC, University of Amsterdam, Department of Intensive Care Medicine, Amsterdam UMC, University of Amsterdam – sequence: 2 givenname: Caitlin surname: Bozic fullname: Bozic, Caitlin organization: Department of Anesthesiology, Amsterdam UMC, VU University, Laboratory for Experimental Intensive Care and Anesthesiology (LEICA), Amsterdam UMC, University of Amsterdam – sequence: 3 givenname: Chantal A. surname: Polet fullname: Polet, Chantal A. organization: Laboratory for Experimental Intensive Care and Anesthesiology (LEICA), Amsterdam UMC, University of Amsterdam, Department of Intensive Care Medicine, Amsterdam UMC, University of Amsterdam – sequence: 4 givenname: Annabel surname: Bongers fullname: Bongers, Annabel organization: Laboratory for Experimental Intensive Care and Anesthesiology (LEICA), Amsterdam UMC, University of Amsterdam, Department of Intensive Care Medicine, Amsterdam UMC, University of Amsterdam – sequence: 5 givenname: Anita M. surname: Tuip-de Boer fullname: Tuip-de Boer, Anita M. organization: Laboratory for Experimental Intensive Care and Anesthesiology (LEICA), Amsterdam UMC, University of Amsterdam, Department of Intensive Care Medicine, Amsterdam UMC, University of Amsterdam – sequence: 6 givenname: Roselique surname: Ibelings fullname: Ibelings, Roselique organization: Department of Anesthesiology, Amsterdam UMC, VU University, Laboratory for Experimental Intensive Care and Anesthesiology (LEICA), Amsterdam UMC, University of Amsterdam, Department of Intensive Care Medicine, Amsterdam UMC, University of Amsterdam – sequence: 7 givenname: Joris J. T. H. surname: Roelofs fullname: Roelofs, Joris J. T. H. organization: Department of Pathology, Amsterdam UMC, University of Amsterdam, Amsterdam Cardiovascular Sciences, University of Amsterdam – sequence: 8 givenname: Nicole P. surname: Juffermans fullname: Juffermans, Nicole P. organization: Laboratory for Experimental Intensive Care and Anesthesiology (LEICA), Amsterdam UMC, University of Amsterdam, Department of Intensive Care Medicine, Amsterdam UMC, University of Amsterdam, OLVG Hospital |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/38778274$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1186_s12871_025_03251_3 crossref_primary_10_1016_j_jep_2025_120070 crossref_primary_10_3390_ijms26073000 |
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| Keywords | Edema Ventilator-induced lung injury Lung ARDS CTGF |
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Acute respiratory distress syndrome (ARDS) is characterized by alveolar edema that can progress to septal fibrosis. Mechanical ventilation can... Acute respiratory distress syndrome (ARDS) is characterized by alveolar edema that can progress to septal fibrosis. Mechanical ventilation can augment lung... BackgroundAcute respiratory distress syndrome (ARDS) is characterized by alveolar edema that can progress to septal fibrosis. Mechanical ventilation can... Abstract Background Acute respiratory distress syndrome (ARDS) is characterized by alveolar edema that can progress to septal fibrosis. Mechanical ventilation... |
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| SubjectTerms | Animals Antibodies Antibodies, Neutralizing - pharmacology ARDS Biomedical and Life Sciences Biomedicine Blood gas analysis Blood pressure Carotid arteries Catheters Connective tissue Connective Tissue Growth Factor - antagonists & inhibitors Connective Tissue Growth Factor - metabolism CTGF Disease Models, Animal Edema Growth factors Ketamine Lung Lung - metabolism Lung - pathology Lungs Male Molecular Medicine Permeability Pulmonary Edema - etiology Pulmonary Edema - metabolism Pulmonary fibrosis Rats Rats, Sprague-Dawley Receptor for Advanced Glycation End Products - antagonists & inhibitors Receptor for Advanced Glycation End Products - metabolism Research Article Ventilator-induced lung injury Ventilator-Induced Lung Injury - drug therapy Ventilator-Induced Lung Injury - metabolism Ventilator-Induced Lung Injury - pathology Ventilators |
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| Title | Effect of antibody-mediated connective tissue growth factor neutralization on lung edema in ventilator-induced lung injury in rats |
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