scholarly journals Lactic acid concentrations in bronchoalveolar lavage fluid correlate with neutrophil influx in cystic fibrosis

2019 ◽  
Vol 1 (1) ◽  
Author(s):  
Keith C Meyer ◽  
Amy Amessoudji ◽  
Trina Hollatz ◽  
Francis HS Tsao
Biomarkers ◽  
2009 ◽  
Vol 14 (1) ◽  
pp. 55-60 ◽  
Author(s):  
Justyna E. Wolak ◽  
Charles R. Esther ◽  
Thomas M. O’Connell

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.


1998 ◽  
Vol 18 (1) ◽  
pp. 120-128 ◽  
Author(s):  
Francis H. C. Tsao ◽  
Keith C. Meyer ◽  
Xiaoming Chen ◽  
Nancy S. Rosenthal ◽  
Junpei Hu

2004 ◽  
Vol 32 (Supplement) ◽  
pp. A115
Author(s):  
Neal J Thomas ◽  
Gavin R Graff ◽  
Todd M Umstead ◽  
David S Phelps ◽  
Joanna Floros

1991 ◽  
Vol 70 (4) ◽  
pp. 1575-1585 ◽  
Author(s):  
G. C. Kindt ◽  
J. E. Gadek ◽  
J. E. Weiland

The adult respiratory distress syndrome and bacterial pneumonia are both characterized by an influx of neutrophils into the lung. The neutrophil has been implicated as having a “pathological” role in adult respiratory distress syndrome, in contrast to its role in bacterial pneumonia. We hypothesized that processes resulting in neutrophil recruitment to the lung are distinct, depending on whether the inflammatory stimulus arises in the intravascular or the alveolar compartment of the lung. Anesthetized sheep with lung lymph fistulas were utilized to access the three compartments of the lung relevant to studies of transpulmonary neutrophil migration. Serum, lung lymph, and bronchoalveolar lavage fluid were studied for neutrophil influx and chemotactic activity before and after administration of endotoxin by either an intravascular or inhaled alveolar route. Both groups developed significant neutrophil influx into the lymph and bronchoalveolar lavage fluid by 3 h postendotoxin. Those animals receiving intravascular endotoxin developed chemotactic gradients opposing neutrophil migration into the lung in contrast to animals receiving alveolar endotoxin, suggesting that neutrophil influx into the lung occurs by random migration.


2009 ◽  
Vol 44 (11) ◽  
pp. 1057-1064 ◽  
Author(s):  
William T. Harris ◽  
Marianne S. Muhlebach ◽  
Robert A. Oster ◽  
Michael R. Knowles ◽  
Terry L. Noah

2007 ◽  
Vol 104 (51) ◽  
pp. 20529-20533 ◽  
Author(s):  
J. K. Harris ◽  
M. A. De Groote ◽  
S. D. Sagel ◽  
E. T. Zemanick ◽  
R. Kapsner ◽  
...  

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