IL-13 stimulates vascular endothelial cell growth factor and protects against hyperoxic acute lung injury

Corne, Jonathan; Chupp, Geoffrey; Lee, Chang-Min; Homer, Robert J.; Zhu, Zhou; Chen, Qingsheng; Ma, Bing; Du, Yuefen; Roux, Françoise; McArdle, John R.; Waxman, Aaron B.; Elias, Jack A.

doi:10.1172/jci9674

Cited by 157 publications

(169 citation statements)

References 46 publications

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“…The sequence of events leading to acute lung injury after exposure to hyperoxia has been described in several different models and the focus of most studies has been on the endothelial cells and epithelial cells of the alveolar wall (7-9, 11, 12). A number of different growth factors and cytokines (IL-6, IL-11, IL-13, keratinocyte growth factor and vascular endothelial cell growth factor) can modify this injury response to hyperoxia (33)(34)(35)(36)(37)(38)(39). TNF-␣ has been found to have a complex role in the pathogenesis of acute lung injury due to hyperoxia (40 -42).…”

Section: Discussionmentioning

confidence: 99%

Sublethal Hyperoxia Impairs Pulmonary Innate Immunity

Baleeiro

Wilcoxen

Morris

et al. 2003

The Journal of Immunology

108

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Supplemental oxygen is often required in the treatment of critically ill patients. The impact of hyperoxia on pulmonary host defense is not well-established. We hypothesized that hyperoxia directly impairs pulmonary host defense, beyond effects on alveolar wall barrier function. C57BL/6 mice were kept in an atmosphere of >95% O2 for 4 days followed by return to room air. This exposure does not lead to mortality in mice subsequently returned to room air. Mice kept in room air served as controls. Mice were intratracheally inoculated with Klebsiella pneumoniae and followed for survival. Alveolar macrophages (AM) were harvested by bronchoalveolar lavage after 4 days of in vivo hyperoxia for ex vivo experiments. Mortality from pneumonia increased significantly in mice exposed to hyperoxia compared with infected mice in room air. Burden of organisms in the lung and dissemination of infection were increased in the hyperoxia group whereas accumulation of inflammatory cells in the lung was impaired. Hyperoxia alone had no impact on AM numbers, viability, or ability to phagocytize latex microbeads. However, following in vivo hyperoxia, AM phagocytosis and killing of Gram-negative bacteria and production of TNF-α and IL-6 in response to LPS were significantly reduced. AM surface expression of Toll-like receptor-4 was significantly decreased following in vivo hyperoxia. Thus sublethal hyperoxia increases Gram-negative bacterial pneumonia mortality and has a significant adverse effect on AM host defense function. Impaired AM function due to high concentrations of supplemental oxygen may contribute to the high rate of ventilator-associated pneumonia seen in critically ill patients.

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Section: Discussionmentioning

confidence: 99%

Sublethal Hyperoxia Impairs Pulmonary Innate Immunity

Baleeiro

Wilcoxen

Morris

et al. 2003

The Journal of Immunology

108

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“…Recent studies from our laboratory and others have added to this pathogenic paradigm by demonstrating that ROS mediate their effects, in part, by inducing an endothelial and epithelial cell death response with features of apoptosis and necrosis 6,20,21,25,36,41,42 and that a variety of exogenously administered regulators inhibit these toxic events by regulating local cell death responses. 5,6,20 In addition, although structural cell apoptosis (such as that seen in HALI) can stimulate tissue inflammation, 43,44 hyperoxia-induced inflammation cannot be attributed solely to the nearby cell death response.…”

Section: © 2 0 0 7 L a N D E S B I O S C I E N C E D O N O T D I S mentioning

confidence: 99%

“…2 Hyperoxia-induced acute lung injury (HALI) is characterized by an extensive inflammatory response and destruction of the alveolarcapillary barrier. [3][4][5][6] The inflammatory cell influx is orchestrated and amplified by chemotactic factors. 7 Morphologic studies in animal models have demonstrated that toxic concentrations of oxygen initially induce focal endothelial cell cytoplasmic swelling and injury and, with continued exposure, necrosis of epithelial cells.…”

Section: Introductionmentioning

confidence: 99%

The Role of Angiopoietin 2 in Hyperoxia-Inuduced Acute Lung Injury

Bhandari¹,

Elias²

2007

Cell Cycle

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“…Administration of a caspase inhibitor has been shown to prevent lethal apoptosis in mice with endotoxin-induced acute lung injury [31]. COMPERNOLLE et al [32] demonstrated a beneficial effect of VEGF administration during respiratory distress syndrome in neonatal mice [32], and CORNE et al [33] found that mice transfected with interleukin 13 during hyperoxia-induced lung injury had an increase in survival that was mediated in part by an increase in VEGF synthesis [33].…”

Section: Vascular Endothelial Growth Factor and Ards Y Abadie Et Almentioning

confidence: 99%

Decreased VEGF concentration in lung tissue and vascular injury during ARDS

Abadie

Brégeon²,

Papazian³

et al. 2005

European Respiratory Journal

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Endothelial injury is an important prognostic factor in acute respiratory distress syndrome (ARDS). Decreased production of vascular endothelial growth factor (VEGF) in ARDS may favour vascular lesions, since VEGF promotes endothelial survival by inhibiting apoptosis.This study sought to document low VEGF levels in lung tissue from ARDS patients, to determine whether the cause was injury to alveolar type II cells (the main pulmonary source of VEGF) and to evaluate the vascular consequences. Lung specimens were obtained by open biopsy or autopsy from 29 patients with severe ARDS (two survivors) and five controls.As compared with controls, homogenates of lung tissue from ARDS patients contained less VEGF (median (interquartile range) ARDS 8.2 (4.7-12.2) versus controls 28.4 (9.9-47.1) ng?g -1 protein). Increased immunostaining with surfactant protein B was seen in ARDS lungs. Extensive cellular apoptosis (terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labelling staining), including endothelial and alveolar type II cells, was demonstrated, and vascular bed density (CD31 immunostaining) decreased in ARDS lungs as compared with controls. VEGF levels were negatively correlated to apoptotic endothelial cell counts.In conclusion, decreased vascular endothelial growth factor levels in lung tissue may participate in the decrease in lung perfusion in acute respiratory distress syndrome.

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IL-13 stimulates vascular endothelial cell growth factor and protects against hyperoxic acute lung injury

Cited by 157 publications

References 46 publications

Sublethal Hyperoxia Impairs Pulmonary Innate Immunity

Sublethal Hyperoxia Impairs Pulmonary Innate Immunity

The Role of Angiopoietin 2 in Hyperoxia-Inuduced Acute Lung Injury

Decreased VEGF concentration in lung tissue and vascular injury during ARDS

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