Resistance To Recombinant Adenovirus Expressing Transforming Growth Factor-ß Correlates With Altered Inflammatory Cytokine Expression In The Bronchoalveolar Lavage Fluid Of Mice That Express Mutant P53 In The Lung Epithelium

2010 ◽  
Author(s):  
James F. Guenther ◽  
Yu Wang ◽  
Bin Shan ◽  
Deborah Sullivan ◽  
Gilbert F. Morris
Keyword(s):  
Growth Factor ◽  
Bronchoalveolar Lavage ◽  
Inflammatory Cytokine ◽  
Bronchoalveolar Lavage Fluid ◽  
Transforming Growth Factor ◽  
Recombinant Adenovirus ◽  
Lavage Fluid ◽  
Cytokine Expression ◽  
Mutant P53 ◽  
Lung Epithelium

Transforming growth factor-β1in bronchoalveolar lavage fluid from children with cystic fibrosis

2009 ◽  
Vol 44 (11) ◽  
pp. 1057-1064 ◽  
Author(s):  
William T. Harris ◽  
Marianne S. Muhlebach ◽  
Robert A. Oster ◽  
Michael R. Knowles ◽  
Terry L. Noah
Keyword(s):  
Cystic Fibrosis ◽  
Growth Factor ◽  
Bronchoalveolar Lavage ◽  
Bronchoalveolar Lavage Fluid ◽  
Transforming Growth Factor ◽  
Lavage Fluid

Expression of mutant human epidermal receptor 3 attenuates lung fibrosis and improves survival in mice

2005 ◽  
Vol 99 (1) ◽  
pp. 298-307 ◽  
Author(s):  
David E. Nethery ◽  
Bethany B. Moore ◽  
George Minowada ◽  
James Carroll ◽  
Jihane A. Faress ◽  
...  
Keyword(s):  
Growth Factor ◽  
Lung Injury ◽  
Transgenic Mice ◽  
Bronchoalveolar Lavage ◽  
Bronchoalveolar Lavage Fluid ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Lavage Fluid ◽  
Dominant Negative ◽  
Nontransgenic Littermate

Neuregulin-1 (NRG-1), binding to the human epidermal growth factor receptor HER2/HER3, plays a role in pulmonary epithelial cell proliferation and recovery from injury in vitro. We hypothesized that activation of HER2/HER3 by NRG-1 would also play a role in recovery from in vivo lung injury. We tested this hypothesis using bleomycin lung injury of transgenic mice incapable of signaling through HER2/HER3 due to lung-specific dominant-negative HER3 (DNHER3) expression. In animals expressing DNHER3, protein leak, cell infiltration, and NRG-1 levels in bronchoalveolar lavage fluid increased after injury, similar to that in nontransgenic littermate control animals. However, HER2/HER3 was not activated, and DNHER3 animals displayed fewer lung morphological changes at 10 and 21 days after injury ( P = 0.01). In addition, they contained 51% less collagen in injured lungs ( P = 0.04). Transforming growth factor-β1 did not increase in bronchoalveolar lavage fluid from DNHER3 mice compared with nontransgenic littermate mice ( P = 0.001), suggesting that a mechanism for the decreased fibrosis was lack of transforming growth factor-β1 induction in DNHER3 mice. Severe lung injury (0.08 units bleomycin) resulted in 80% mortality of nontransgenic mice, but only 35% mortality of DNHER3 transgenic mice ( P = 0.04). Thus inhibition of HER2/HER3 signaling protects against pulmonary fibrosis and improves survival.

Desoxyrhapontigenin Modulates Immunity and Inflammation in an Ovalbumin-Induced Rat Model of Asthma

2021 ◽  
Vol 20 (1) ◽  
pp. 22-27
Author(s):  
Zhaowen Shi ◽  
Xuming Luo
Keyword(s):  
Growth Factor ◽  
Bronchoalveolar Lavage ◽  
Rat Model ◽  
Bronchoalveolar Lavage Fluid ◽  
Transforming Growth Factor ◽  
Present Report ◽  
Lavage Fluid ◽  
Transforming Growth Factor Β1 ◽  
Pronounced Increase ◽  
Rat Tissue

Asthma is a state of hyperresponsiveness of airways with associated inflammation and obstruction to air track. Present report evaluated the protective effect of desoxyrhapontigenin against ovalbumin-induced rat model of asthma. In asthmatic rats, there was an increase in serum IL-4, IL-5, bronchoalveolar lavage fluid IgE, IL-4, IL-13, IL-17, transforming growth factor β1, and leucocyte count. On the contrary, there was a decrease in bronchoalveolar lavage fluid IFN-γ that was reversed by desoxyrhapontigenin but not dexomethasone. Also, the mRNA expression for NF-kBp65 and vascular endothelial growth factor increased without any change in IκBα in the asthmatic rat tissue. There was a pronounced increase in the histopathological score in asthmatic rat tissue that were diminished by desoxyrhapontigenin or dexomethasone. In conclusion, study reveals that treatment with desoxyrhapontigen may protect the bronchial asthma by modulating the inflammation and immune response in the lung tissue.

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.

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