Airway injury in an in vitro human epithelium-fibroblast model of diacetyl vapor exposure: diacetyl-induced basal/suprabasal spongiosis

2017 ◽  
Vol 29 (7) ◽  
pp. 310-321 ◽  
Author(s):  
William M. Gwinn ◽  
Gordon P. Flake ◽  
Ronald W. Bousquet ◽  
Genie J. Taylor ◽  
Daniel L. Morgan
Keyword(s):  
Airway Injury ◽  
Fibroblast Model

scholarly journals In-vivo efficacy of biodegradable ultrahigh ductility Mg-Li-Zn alloy tracheal stents for pediatric airway obstruction

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Jingyao Wu ◽  
Leila J. Mady ◽  
Abhijit Roy ◽  
Ali Mübin Aral ◽  
Boeun Lee ◽  
...  
Keyword(s):  
Degradation Products ◽  
Metallic Matrix ◽  
Management Technique ◽  
Pediatric Airway ◽  
Endoscopic Techniques ◽  
Airway Stent ◽  
Airway Injury ◽  
Life Threatening

AbstractPediatric laryngotracheal stenosis is a complex congenital or acquired airway injury that may manifest into a potentially life-threatening airway emergency condition. Depending on the severity of obstruction, treatment often requires a combination of endoscopic techniques, open surgical repair, intraluminal stenting, or tracheostomy. A balloon expandable biodegradable airway stent maintaining patency while safely degrading over time may address the complications and morbidity issues of existing treatments providing a less invasive and more effective management technique. Previous studies have focused on implementation of degradable polymeric scaffolds associated with potentially life-threatening pitfalls. The feasibility of an ultra-high ductility magnesium-alloy based biodegradable airway stents was demonstrated for the first time. The stents were highly corrosion resistant under in vitro flow environments, while safely degrading in vivo without affecting growth of the rabbit airway. The metallic matrix and degradation products were well tolerated by the airway tissue without exhibiting any noticeable local or systemic toxicity.

scholarly journals ID2008 Aerosol-based cell delivery as an innovative treatment for lung diseases

2017 ◽  
Vol 4 (S) ◽  
pp. 41 ◽  
Author(s):  
Badrul Hisham Yahaya
Keyword(s):  
Epithelial Cells ◽  
Cell Therapy ◽  
Airway Epithelial Cells ◽  
Cell Delivery ◽  
Airway Epithelial ◽  
Promising Alternative ◽  
Airway Injury ◽  
Lung Injuries ◽  
And Function

Endogenous repair mechanism of airway epithelial cells often fails to achieve sufficient cellular turnover and diminish with age, thus leading to permanent alterations in the structure and function of the airway epithelium. The therapeutic use of stem cells and progenitor cells represents a promising alternative for clinical strategy in treating acute and chronic lung disorders. Aerosol-based cell therapy is a novel therapeutic strategy in enhancing reparative process following both acute and chronic lung injuries. In such background, this study was aimed to determine the effect of aerosol-based cell delivery using MicroSprayer® Aerosolizer in the setting of acute lung injury (ALI) and ovalbumin-induced airway injury in the rabbit. In vitro evaluation revealed that the aerosol technique didn’t cause a significant effect on cell morphology, viability and proliferation capability over the course of cell culture period. Aerosol delivery of airway epithelial cells (AEC) and mesenchymal stem cell (MSC) resulted in uniform distribution in the distal airway and lung interstitial region. Short term assessment showed that cells delivered to the lungs via aerosol was found to be safe for transplantation with no signs of cell rejection and histopathological alterations in the liver and spleen of all treated animals. Histological evidences also demonstrated that administration of AEC and MSC via aerosolization into the respiratory airway prevented lung inflammation as well as resulted in improvement of both alveolar damage and permeability. To our knowledge, this is the first report of aerosol cell delivery via a Microsprayer® Aerosolizer device to the lungs of rabbits to treat airway injuries. Our findings provide a promising evidence that aerosol-based cell therapy may provide a basis for the development of an innovative approach for the treatment lung injuries.

scholarly journals ω-3 Polyunsaturated fatty acids accelerate airway repair by activating FFA4 in club cells

2017 ◽  
Vol 312 (6) ◽  
pp. L835-L844 ◽  
Author(s):  
Kyoung-Pil Lee ◽  
Soo-Jin Park ◽  
Saeromi Kang ◽  
Jung-Min Koh ◽  
Koichi Sato ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Epithelial Cells ◽  
Polyunsaturated Fatty Acids ◽  
Knockout Mice ◽  
Airway Injury ◽  
Club Cells ◽  
And Migration ◽  
Lung Health

A G protein-coupled receptor (GPCR) named free fatty acid receptor 4 (FFA4, also known as GPR120) was found to act as a GPCR for ω-3 polyunsaturated fatty acids. Its expression has been reported in lung epithelial club cells. We investigated whether supplementation of the ω-3 fatty acids benefits lung health. Omacor (7.75 mg/kg), clinically prescribed preparation of ω-3 fatty acids, and FFA4-knockout mice were utilized in a naphthalene-induced mouse model of acute airway injury (1 injection of 30 mg/kg ip). Naphthalene injection induced complete destruction of bronchiolar epithelial cells within a day. Appearance of bronchiolar epithelial cells was observed after 21 days in control mice. It was found, however, that supplementation of Omacor accelerated the recovery. The appearance of bronchiolar epithelial cells was observed between 7 and 14 days after naphthalene injury in Omacor-treated mice. In isolated club cells, ω-3 fatty acids were found to stimulate cell proliferation and migration but to inhibit cell differentiation. With the use of pharmacological tools and FFA4-knockout mice, FFA4 was found to be responsible for ω-3 fatty acids-induced proliferation in vitro in club cells. Furthermore, accelerated recovery from naphthalene-induced airway injury in Omacor-treated mice was not observed in FFA4-knockout mice in vivo. Present findings indicate that ω-3 fatty acids-induced proliferation of bronchiole epithelial cells through FFA4 is responsible for Omacor-induced accelerated recovery from airway injury. Therefore, intermittent administration of Omacor needs to be tested for acute airway injury because ω-3 fatty acids stimulate proliferation but inhibit differentiation of club cells.

Transforming growth factor-β1 increases airway wound repair via MMP-2 upregulation: a new pathway for epithelial wound repair?

2006 ◽  
Vol 290 (6) ◽  
pp. L1277-L1282 ◽  
Author(s):  
E. Lechapt-Zalcman ◽  
V. Prulière-Escabasse ◽  
D. Advenier ◽  
S. Galiacy ◽  
C. Charrière-Bertrand ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Wound Repair ◽  
Transforming Growth Factor ◽  
Airway Epithelial ◽  
Airway Injury ◽  
Tgf Β1

In vivo, transforming growth factor (TGF)-β1 and matrix metalloproteinases (MMPs) present at the site of airway injury are thought to contribute to epithelial wound repair. As TGF-β1 can modulate MMP expression and MMPs play an important role in wound repair, we hypothesized that TGF-β1 may enhance airway epithelial repair via MMPs secreted by epithelial cells. We evaluated the in vitro influence of TGF-β1 on wound repair in human airway epithelial cells cultured under conditions allowing differentiation. The results showed that TGF-β1 accelerated in vitro airway wound repair, whereas MMP inhibitors prevented this acceleration. In parallel, we examined the effect of TGF-β1 on the expression of MMP-2 and MMP-9. TGF-β1 induced a dramatic increase of MMP-2 expression with an increased steady-state level of MMP-2 mRNA, contrasting with a slight increase in MMP-9 expression. To confirm the role of MMP-2, we subsequently evaluated the effect of MMP-2 on in vitro airway wound repair and demonstrated that the addition of MMP-2 reproduced the acceleration of wound repair induced by TGF-β1. These results strongly suggest that TGF-β1 increases in vitro airway wound repair via MMP-2 upregulation. It also raises the issue of a different in vivo biological role of MMP-2 and MMP-9 depending on the cytokine microenvironment.

Early high expression of IP-10 in F344 rats resistant to Sendai virus-induced airway injury

2003 ◽  
Vol 285 (6) ◽  
pp. L1263-L1269 ◽  
Author(s):  
Xuezhong Cai ◽  
William L. Castleman
Keyword(s):  
Epithelial Cells ◽  
Sendai Virus ◽  
Interferon Γ ◽  
Airway Epithelial Cells ◽  
Early Gene ◽  
High Expression ◽  
Suppressive Subtractive Hybridization ◽  
Airway Injury ◽  
F344 Rats

Weanling F344 and BN rats differ markedly in their susceptibility to Sendai virus-induced airway injury. Early gene expression that controls their differences in susceptibility remains poorly understood. In this study we combined suppressive subtractive hybridization and cDNA library array hybridization to identify genes differentially expressed in virus-susceptible BN and virus-resistant F344 rats during the first 3 days after inoculation. Differential expression of selected clones was further verified by quantitative RT-PCR. Seven virus-induced gene segments were identified. Of them, interferon-γ-inducible protein 10 (IP-10), Mx1, and guany-late-binding protein-2 mRNA abundance in infected F344 rats was 201.5, 188.2, and 281.7% higher, respectively, than that of infected BN rats at 2 days after inoculation. In situ hybridization indicated that virus-induced IP-10 was expressed mainly in airway epithelial cells of F344 rats. Sendai virus infection can directly induce IP-10 expression in rat tracheal epithelial cells in vitro. IP-10 early high expression might contribute to the resistance to virus-induced airway disease in F344 rats by promoting Th1 responses and increasing antiviral activity.

THE TAY-SACHS DISEASE FIBROBLAST MODEL: FAILURE TO RESPOND TO EXOGENOUS HEXOSAMINIDASE A

PEDIATRICS ◽  
1973 ◽  
Vol 52 (2) ◽  
pp. 221-226
Author(s):  
Larry Schneck ◽  
Daniel Amsterdam ◽  
Steven E. Brooks ◽  
Arthur L. Rosenthal ◽  
Bruno W. Volk
Keyword(s):  
Cultured Cells ◽  
In Vitro Studies ◽  
Parenteral Administration ◽  
Fluorogenic Substrate ◽  
Fibroblast Cultures ◽  
Tay Sachs Disease ◽  
Hexosaminidase A ◽  
Model Failure ◽  
Fibroblast Model

In vitro studies with Tay-Sachs disease (TSD) fibroblast cultures treated with β-D-N-acetylhexosaminidase A (Hex A) did not reveal any detectable incorporation of the enzyme into cultured cells as measured by activity against the fluorogenic substrate or intracellular radioactivity of the 125I-labeled enzyme. Futhermore, there was no demonstrable alteration of 14C-labeled GM2 (TSD) ganglioside in treated cells. It was concluded that parenteral administration of this enzyme to affected infants is not clinically justifiable.

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