Vascular endothelial growth factor in patients with high-altitude pulmonary edema

2003 ◽  
Vol 94 (5) ◽  
pp. 1836-1840 ◽  
Author(s):  
Masayuki Hanaoka ◽  
Yunden Droma ◽  
Atsuhiko Naramoto ◽  
Takayuki Honda ◽  
Toshio Kobayashi ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage ◽  
Pulmonary Edema ◽  
High Altitude ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Repair Process ◽  
Vascular Endothelial ◽  
High Altitude Pulmonary Edema ◽  
Endothelial Growth Factor

To examine the role of VEGF in the pathogenesis of high-altitude pulmonary edema (HAPE), we measured the concentrations of VEGF in venous serum and bronchoalveolar lavage fluid in patients with HAPE and in healthy volunteers. The VEGF in venous serum of the patients was normal at admission and significantly increased at recovery. Similarly, the VEGF in bronchoalveolar lavage fluid of the patients was increased at recovery compared with admission, but values at both admission and recovery were significantly lower than those of the controls. The present finding suggests that VEGF probably is destroyed in the lung of HAPE, and it appears less likely to have a critical part in the pathogenesis of HAPE but has rather an important role in the repair process for the impaired cell layer.

scholarly journals Vascular Endothelial Growth Factor in Bronchoalveolar Lavage Fluid in Sulfur Mustard Exposed Lung Patients

2011 ◽  
Vol 26 (2) ◽  
pp. 118-121 ◽  
Author(s):  
Ali Karami ◽  
Mostafa Ghanei ◽  
Farshid Alaeddini ◽  
Mohammad Javad Soltanpour ◽  
Fatemeh Pourali ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Bronchoalveolar Lavage ◽  
Bronchoalveolar Lavage Fluid ◽  
Sulfur Mustard ◽  
Lavage Fluid ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

scholarly journals Vascular Endothelial Growth Factor‐121 Administration Mitigates Halogen Inhalation‐Induced Pulmonary Injury and Fetal Growth Restriction in Pregnant Mice

2020 ◽  
Vol 9 (3) ◽  
Author(s):  
Dylan R. Addis ◽  
James A. Lambert ◽  
Changchun Ren ◽  
Stephen Doran ◽  
Saurabh Aggarwal ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Bronchoalveolar Lavage ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Vascular Endothelial ◽  
Pregnant Mice ◽  
Endothelial Growth Factor

Background Circulating levels of sFLT‐1 (soluble fms‐like tyrosine kinase 1), the extracellular domain of vascular endothelial growth factor (VEGF) receptor 1, and its ratio to levels of placental growth factor are markers of the occurrence and severity of preeclampsia. Methods and Results C57BL/6 pregnant mice on embryonic day 14.5 (E14.5), male, and non‐pregnant female mice were exposed to air or to Br 2 at 600 ppm for 30 minutes and were treated with vehicle or with VEGF‐121 (100 μg/kg, subcutaneously) daily, starting 48 hours post‐exposure. Plasma, bronchoalveolar lavage fluid, lungs, fetuses, and placentas were collected 120 hours post‐exposure. In Br 2 ‐exposed pregnant mice, there was a time‐dependent and significant increase in plasma levels of sFLT‐1 which correlated with increases in mouse lung wet/dry weights and bronchoalveolar lavage fluid protein content. Supplementation of exogenous VEGF‐121 improved survival and weight gain, reduced lung wet/dry weights, decreased bronchoalveolar lavage fluid protein levels, enhanced placental development, and improved fetal growth in pregnant mice exposed to Br 2 . Exogenous VEGF‐121 administration had no effect in non‐pregnant mice. Conclusions These results implicate inhibition of VEGF signaling driven by sFLT‐1 overexpression as a mechanism of pregnancy‐specific injury leading to lung edema, maternal mortality, and fetal growth restriction after bromine gas exposure.

scholarly journals 2045 The role of TGFβ in driving early cystic fibrosis lung disease

2018 ◽  
Vol 2 (S1) ◽  
pp. 33-33
Author(s):  
Elizabeth L. Kramer ◽  
William Hardie ◽  
Kristin Hudock ◽  
Cynthia Davidson ◽  
Alicia Ostmann ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Bronchoalveolar Lavage ◽  
Lung Disease ◽  
Bronchoalveolar Lavage Fluid ◽  
Transforming Growth Factor ◽  
Genetic Modifier ◽  
Lavage Fluid ◽  
Lung Mechanics ◽  
Patient Specific

OBJECTIVES/SPECIFIC AIMS: Transforming growth factor-beta (TGFβ) is a genetic modifier of cystic fibrosis (CF) lung disease. TGFβ’s pulmonary levels in young CF patients and its mechanism of action in CF are unknown. We examined TGFβ levels in children with CF and investigated responses of human airway epithelial cells (AECs) and mice to TGFβ. METHODS/STUDY POPULATION: TGFβ levels in bronchoalveolar lavage fluid from CF patients (n=15) and non-CF control patients (n=21)<6 years old were determined by ELISA. CF mice and non-CF mice were intratracheally treated with an adenoviral TGFβ1 vector or PBS; lungs were collected for analysis at day 7. Human CF and non-CF AECs were treated with TGFβ or PBS for 24 hours then collected for analysis. RESULTS/ANTICIPATED RESULTS: Young CF patients had higher bronchoalveolar lavage fluid TGFβ than non-CF controls (p=0.03). Mouse lungs exposed to TGFβ demonstrated inflammation, goblet cell hyperplasia, and decreased CFTR expression. CF mice had greater TGFβ-induced lung mechanics abnormalities than controls; both CF human AECs and CF mice showed higher TGFβ induced MAPK and PI3K signaling compared with controls. DISCUSSION/SIGNIFICANCE OF IMPACT: For the first time, we show increased TGFβ levels very early in CF. TGFβ drives CF lung abnormalities in mouse and human models; CF models are more sensitive to TGFβ’s effects. Understanding the role of TGFβ in promoting CF lung disease is critical to developing patient specific treatments.

Interaction of bronchoalveolar lavage fluid with polyplexes and lipoplexes: analysing the role of proteins and glycoproteins

2002 ◽  
Vol 5 (1) ◽  
pp. 49-60 ◽  
Author(s):  
J. Rosenecker ◽  
S. Naundorf ◽  
S. W. Gersting ◽  
R. W. Hauck ◽  
A. Gessner ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid

scholarly journals Role of bronchoalveolar lavage fluid and serum interleukin-27 in the diagnosis of smear-negative pulmonary tuberculosis

Medicine ◽  
2021 ◽  
Vol 100 (20) ◽  
pp. e25821
Author(s):  
Feng Zhu ◽  
Qinfang Ou ◽  
Jian Zheng ◽  
Min Zhou ◽  
Huaxin Chen ◽  
...  
Keyword(s):  
Pulmonary Tuberculosis ◽  
Bronchoalveolar Lavage ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Interleukin 27 ◽  
Smear Negative

scholarly journals Oxidative and Proteolytic Inactivation of Alpha-1 Antitrypsin in Bronchopulmonary Dysplasia Pathogenesis: A Top-Down Proteomic Bronchoalveolar Lavage Fluid Analysis

2021 ◽  
Vol 9 ◽  
Author(s):  
Chiara Tirone ◽  
Federica Iavarone ◽  
Milena Tana ◽  
Alessandra Lio ◽  
Claudia Aurilia ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage ◽  
Bronchopulmonary Dysplasia ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Small Sample ◽  
Preterm Neonates ◽  
Ionization Mass ◽  
Top Down ◽  
Alpha 1 Antitrypsin

The study investigates the role of the oxidative and proteolytic inactivation of alpha-1 antitrypsin (AAT) in the pathogenesis of bronchopulmonary dysplasia (BPD) in premature infants. Bronchoalveolar lavage fluid (BALF) samples were collected on the 3rd day of life from mechanically ventilated neonates with gestational age ≤ 30 weeks and analyzed without previous treatment (top-down proteomics) by reverse-phase high-performance liquid chromatography-electrospray ionization mass spectrometry. AAT fragments were identified by high-resolution LTQ Orbitrap XL experiments and the relative abundances determined by considering the extracted ion current (XIC) peak area. Forty preterm neonates were studied: 20 (50%) did not develop BPD (no-BPD group), 17 (42.5%) developed mild or moderate new-BPD (mild + moderate BPD group), and 3 (7.5%) developed severe new-BPD (severe BPD group). Eighteen fragments of AAT and a fragment of AAT oxidized at a methionine residue were identified: significantly higher values of AAT fragments 25–57, 375–418, 397–418, 144–171, and 397–418 with oxidized methionine were found in the severe BPD group. The significantly higher levels of several AAT fragments and of the fragment 397–418, oxidized in BALF of preterm infants developing BPD, underlie the central role of an imbalance between proteases and protease inhibitors in exacerbating lung injury and inducing most severe forms of BPD. The study has some limitations, and between them, the small sample size implies the need for further confirmation by larger studies.

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