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 ◽  
...  
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.


Medicine ◽  
2021 ◽  
Vol 100 (20) ◽  
pp. e25821
Author(s):  
Feng Zhu ◽  
Qinfang Ou ◽  
Jian Zheng ◽  
Min Zhou ◽  
Huaxin Chen ◽  
...  

2021 ◽  
Vol 9 ◽  
Author(s):  
Chiara Tirone ◽  
Federica Iavarone ◽  
Milena Tana ◽  
Alessandra Lio ◽  
Claudia Aurilia ◽  
...  

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.


2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Cynthia Pessoa Neves ◽  
Allyson Guimarães Costa ◽  
Izabella Picinin Safe ◽  
Alexandra de Souza Brito ◽  
Jaquelane Silva Jesus ◽  
...  

2010 ◽  
Vol 54 (3) ◽  
pp. 296-302 ◽  
Author(s):  
Rashmi Gupta ◽  
Venkateswaran K. Iyer ◽  
Bijay Ranjan Mirdha ◽  
Randeep Guleria ◽  
Lalit Kumar ◽  
...  

2003 ◽  
Vol 12 (4) ◽  
pp. 209-214 ◽  
Author(s):  
Agnès Hamzaoui ◽  
Jamel Ammar ◽  
Hédia Graïri ◽  
Kamel Hamzaoui

Objective:To understand the role of apoptosis through Fas/Fas ligand (FasL) interaction in the pathogenesis of silicosis, we examined the expression of Fas antigen, FasL and apoptosis in bronchoalveolar lavage fluid lymphocytes obtained from patients with silicosis.Materials and methods:Ten patients with silicosis, and 10 healthy controls were studied. Non-adherent cells were separated and analysed by cytometry for the expression of Fas antigen, FasL, and the co-expression of Fas/FasL. By double staining, we studied the FasL expression on CD4, CD8, CD56 and CD45RO-positive cells. DNA fragmentation was investigated by the terminal deoxy(d) UTP nick end labelling (TUNEL) method.Results:We have found Fas and FasL expression in silicosis patients to be significantly higher than those in healthy controls. Interestingly, 6-18% of lymphocytes from silicosis patients co-expressed Fas and FasL. In silicosis patients, FasL was highly expressed on CD4+, CD56+and CD45RO+bronchoalveolar lavage cells. Fas antigen expressing cells showed DNA fragmentation characteristic for apoptosis.Conclusion:FasL was significantly expressed on cytotoxic effector and memory cells. The Fas/FasL system is implicated in the inflammatory process observed in silicosis patients.


Author(s):  
Satish Chandra Kilaru ◽  
Nagender Prasad Chenimilla ◽  
Umair Syed ◽  
Kashif Momin ◽  
Hemanth Kilaru ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document