Imbalance in the Expression of CXC Chemokines Correlates with Bronchoalveolar Lavage Fluid Angiogenic Activity and Procollagen Levels in Acute Respiratory Distress Syndrome

Keane, Michael P.; Donnelly, Seamas C.; Belperio, John A.; Goodman, Richard B.; Dy, Maria; Burdick, Marie D.; Fishbein, Michael C.; Strieter, Robert M.

doi:10.4049/jimmunol.169.11.6515

Cited by 59 publications

(53 citation statements)

References 39 publications

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“…In contrast, while BALF levels of VEGF were elevated in ARDS patients, VEGF did not appear to be a predominant factor in contributing to the overall angiogenic activity (92). Taken together, these findings support the notion that angiogenesis is critical to promote fibroplasia and deposition of ECM associated with chronic fibroproliferation, and that angiogenic and angiostatic factors, such as CXC chemokines play an important role in the pathogenesis of this process.…”

Section: Chemokine-induced Angiogenesis In Inflammatory and Fibroprolsupporting

confidence: 48%

“…Acute respiratory distress syndrome (ARDS) is a common and severe manifestation of acute lung injury, and progresses to a fibroproliferative phase after several days, which is associated with marked angiogenesis related to ELR+ CXC chemokines (92): BALF from patients with ARDS has elevated levels of angiogenic chemokines and reduced levels of angiostatic chemokines, as compared to control ventilated patients without ARDS, and this was associated with BALF angiogenic activity and BALF pro-collagen I and pro-collagen III levels (92). In contrast, while BALF levels of VEGF were elevated in ARDS patients, VEGF did not appear to be a predominant factor in contributing to the overall angiogenic activity (92).…”

Section: Chemokine-induced Angiogenesis In Inflammatory and Fibroprolmentioning

confidence: 99%

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Chemokines as mediators of angiogenesis

Mehrad¹,

Keane²,

Strieter³

2007

Thromb Haemost

181

145

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SummaryChemokines were originally described as cytokines that mediate leukocyte recruitment to sites of inflammation. Members of a subgroup of chemokines, the CXC family, also play a critical role in both physiologic and pathologic angiogenesis, including in the context of chronic inflammation, fibrosis, and malignancy. A unique feature of this family of cytokines is that, on the basis of their structure and receptor binding, individual ligands display either angiogenic or angiostatic biological activity in the regulation of angiogenesis. In this review, we summarize the key literature in this growing field.

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Section: Chemokine-induced Angiogenesis In Inflammatory and Fibroprolsupporting

confidence: 48%

Section: Chemokine-induced Angiogenesis In Inflammatory and Fibroprolmentioning

confidence: 99%

Chemokines as mediators of angiogenesis

Mehrad¹,

Keane²,

Strieter³

2007

Thromb Haemost

181

145

View full text Add to dashboard Cite

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“…Accordingly, increased VEGF levels in the alveolar space may reflect recovery from ARDS (37). In contrast to these studies, Keane et al (40) suggested that VEGF did not appear to contribute significantly to the angiogenic activity in ARDS, whereas CXC chemokines did. VEGF may indirectly enhance angiogenesis in inflammatory lesions through the up-regulation of chemokines in bleomycin-induced pneumopathy in mice.…”

Section: Discussionmentioning

confidence: 62%

Anti-Vascular Endothelial Growth Factor Gene Therapy Attenuates Lung Injury and Fibrosis in Mice

Hamada

Kuwano

Yamada

et al. 2005

The Journal of Immunology

160

110

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Vascular endothelial growth factor (VEGF) is an angiogenesis factor with proinflammatory roles. Flt-1 is one of the specific receptors for VEGF, and soluble flt-1 (sflt-1) binds to VEGF and competitively inhibits it from binding to the receptors. We examined the role of VEGF in the pathophysiology of bleomycin-induced pneumopathy in mice, using a new therapeutic strategy that comprises transfection of the sflt-1 gene into skeletal muscles as a biofactory for anti-VEGF therapy. The serum levels of sflt-1 were significantly increased at 3–14 days after the gene transfer. Transfection of the sflt-1 gene at 3 days before or 7 days after the intratracheal instillation of bleomycin decreased the number of inflammatory cells, the protein concentration in the bronchoalveolar lavage fluid and with von Willebrand factor expression at 14 days. Transfection of the sflt-1 gene also attenuated pulmonary fibrosis and apoptosis at 14 days. Since the inflammatory cell infiltration begins at 3 days and is followed by interstitial fibrosis, it is likely that VEGF has important roles as a proinflammatory, a permeability-inducing, and an angiogenesis factor not only in the early inflammatory phase but also in the late fibrotic phase. Furthermore, this method may be beneficial for treating lung injury and fibrosis from the viewpoint of clinical application, since it does not require the use of a viral vector or neutralizing Ab.

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“…Interestingly, acute endothelial injury has been reported to be more pronounced at the proliferative phase than at the exudative phase of ARDS [11]. Although VEGF levels are low in the bronchoalveolar lavage fluids of ARDS patients, an increase in angiogenic activity related mainly to CXC chemokines has been reported in one study [17].…”

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

confidence: 97%

Decreased VEGF concentration in lung tissue and vascular injury during ARDS

Abadie

Brégeon²,

Papazian³

et al. 2005

Eur Respir J

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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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Imbalance in the Expression of CXC Chemokines Correlates with Bronchoalveolar Lavage Fluid Angiogenic Activity and Procollagen Levels in Acute Respiratory Distress Syndrome

Cited by 59 publications

References 39 publications

Chemokines as mediators of angiogenesis

Chemokines as mediators of angiogenesis

Anti-Vascular Endothelial Growth Factor Gene Therapy Attenuates Lung Injury and Fibrosis in Mice

Decreased VEGF concentration in lung tissue and vascular injury during ARDS

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