Bronchoalveolar lavage fluid proteins in human lung disease: Analysis by two-dimensional electrophoresis

1993 ◽  
Vol 14 (1) ◽  
pp. 242-244 ◽  
Author(s):  
Anke-Gabriele Lenz ◽  
Barbara Meyer ◽  
Ulrich Costabel ◽  
Konrad Maier
1990 ◽  
Vol 11 (6) ◽  
pp. 510-513 ◽  
Author(s):  
Anke-Gabriele Lenz ◽  
Barbara Meyer ◽  
Hans Weber ◽  
Konrad Maier

2018 ◽  
Vol 2 (S1) ◽  
pp. 33-33
Author(s):  
Elizabeth L. Kramer ◽  
William Hardie ◽  
Kristin Hudock ◽  
Cynthia Davidson ◽  
Alicia Ostmann ◽  
...  

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.


2018 ◽  
Vol 67 (4) ◽  
pp. 761-766
Author(s):  
Li Wei ◽  
Jing Zhao ◽  
Jing Bao ◽  
Yanliang Ma ◽  
Ying Shang ◽  
...  

To investigate the expression and clinical significance of secretory mucins in patients with interstitial lung disease (ILD). The bronchoalveolar lavage fluid (BALF) concentrations of mucins (MUCs) from 27 patients with ILD, 6 patients with lung cancer, 8 patients with pleural effusion and 9 patients with bronchiectasis were determined by ELISA. The concentration of MUC5AC was significantly increased in patients with ILD (12.84±15.02 ng/mL) compared with patients with pleural effusion (4.33±2.51 ng/mL), lung cancer (8.02±5.57 ng/mL) or bronchiectasis (6.08±2.40 ng/mL) (p<0.01). The MUC2 level (10.23±9.27 ng/mL) was significantly elevated in patients with ILD than in those with pleural effusion (6.21±3.28 ng/mL) or bronchiectasis (5.73±1.51 ng/mL) (both p<0.05). Patients with ILD (104.64±61.61 ng/mL), lung cancer (148.45±169.24 ng/mL) or bronchiectasis (123.68±63.28 ng/mL) had significantly greater IL-8 levels than in those with pleural effusion (76.46±2.16 ng/mL) (p<0.05). A significant positive correlation was detected between the MUC5AC concentration and the lymphocyte percentage in BALF of patients with ILD (r=0.504, p=0.007). Lung function tests of patients with ILD exhibited various degrees of restrictive ventilation dysfunction and reduced diffusing capacity. The MUC5AC levels in BALF were negatively correlated with forced expiratory volume in 1 second (FEV1)/forced vital capacity (r=−0.761, p=0.000), FEV1 predicted value (FEV1/pred) (r=−0.668, p=0.002), and diffusing capacity (r=−0.606, p=0.006). Secretory mucins MUC5AC, MUC2 and IL-8 were highly expressed in ILD. MUC5AC level was closely correlated with the amount of inflammatory cells in BALF and the lung function parameters.


1991 ◽  
Vol 81 (3) ◽  
pp. 439-446 ◽  
Author(s):  
F. J. Kelly ◽  
G. I. Town ◽  
G. J. Phillips ◽  
S. T. Holgate ◽  
W. R. Roche ◽  
...  

1. Research into the pathogenesis of acute and chronic neonatal lung disease has been hampered by the lack of a suitable small-animal model of prematurity. We describe such a model that has been developed and validated in the guinea-pig. 2. Pre-term guinea-pigs delivered by Caesarian section at 65 days gestation (normal gestation 68 days) exhibited transient respiratory distress. The survival of pre-term animals was lower than that of term animals after exposure to 95% O2 (pre-term 42% versus term 79% at 96 h, P < 0.05). 3. Pulmonary histology in pre-term animals exposed to both 21% O2 and 95% O2 revealed evidence of acute lung injury with atelectasis, pulmonary oedema, fibrin deposition and inflammatory cell infiltration. No evidence of lung injury was observed in term animals exposed to 21% O2, whereas those exposed to 95% O2 showed a similar, but less pronounced, injury to that seen in preterm pups. 4. The protein concentration in bronchoalveolar lavage fluid was similar in pre-term and term animals exposed to 95% O2, but neutrophil numbers in bronchoalveolar lavage fluid tended to be greater in preterm pups. 5. Elastase-like activity, measured against succinyl-1-trialanine p-nitroanilide, was higher in bronchoalveolar lavage fluid from control pre-term animals compared with that from control term animals. Exposure to 95% O2 increased the elastase-like activity significantly in both groups. The majority of the elastase-like activity was EDTA-sensitive and thus is possibly due to metallo-elastase. Fractionation of bronchoalveolar lavage fluid indicated that the elastase-like activity was associated with a high-molecular-mass complex. Lipase treatment reduced the activity of this fraction and generated a new 40 kDa fraction. 6. We conclude that the pre-term guinea-pig is more susceptible than the term animal to lung injury after O2 exposure and thus represents a appropriate small-animal model in which to investigate the pathogenesis of acute and chronic lung injury in the pre-term infant.


2011 ◽  
Vol 301 (4) ◽  
pp. L510-L518 ◽  
Author(s):  
Elizabeth F. Redente ◽  
Kristen M. Jacobsen ◽  
Joshua J. Solomon ◽  
Abigail R. Lara ◽  
Sarah Faubel ◽  
...  

Fibrotic interstitial pneumonias are more prevalent in males of advancing age, although little is known about the underlying mechanisms. To evaluate the contributions of age and sex to the development of pulmonary fibrosis, we intratracheally instilled young (8–12 wk) and aged (52–54 wk) male and female mice with bleomycin and assessed the development and severity of fibrotic lung disease by measurements of lung collagen levels, static compliance, leukocyte infiltration, and stereological quantification of fibrotic areas in histological sections. We also quantified proinflammatory and profibrotic chemokine and cytokine levels in the bronchoalveolar lavage fluid. Aged male mice developed more severe lung disease, indicated by increased mortality, increased collagen deposition, and neutrophilic alveolitis compared with aged female mice or young mice of either sex. Aged male mice also exhibited increased levels of transforming growth factor-β, IL-17A, and CXCL1 in their bronchoalveolar lavage fluid. Young male mice developed a more fibrotic disease after bleomycin instillation compared with female mice, regardless of age. There was no difference in fibrosis between young and aged female mice. Taken together, these findings suggest that the variables of advanced age and male sex contribute to the severity of pulmonary fibrosis in this model. Our findings also emphasize the importance of stratifying experimental groups on the basis of age and sex in experimental and epidemiological studies of this nature.


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