scholarly journals An Adhesive-Based Fabrication Technique for Culture of Lung Airway Epithelial Cells with Applications in Microfluidics and Lung-on-a-Chip

2020 ◽  
Author(s):  
Nicholas Tiessen ◽  
Mohammadhossein Dabaghi ◽  
Quynh Cao ◽  
Abiram Chandiramohan ◽  
P. Ravi Selvaganapathy ◽  
...  
Keyword(s):  
Cell Culture ◽  
Microfluidic Chip ◽  
Inflammatory Responses ◽  
Cost Effective ◽  
Culture Method ◽  
Porous Membrane ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Culture Cells ◽  
Microfluidic Cell Culture

1AbstractThis work describes a versatile and cost-effective cell culture method for growing adherent cells on a porous membrane using pressure-sensitive double-sided adhesives. This technique allows cell culture using conventional methods and easy transfer to microfluidic chip devices. To support the viability of our system, we evaluate the toxicity effect of four different adhesives on two distinct airway epithelial cell lines and show functional applications for microfluidic cell culture chip fabrication. We showed that cells could be grown and expanded on a “floating” membrane, which can be transferred upon cell confluency to a microfluidic chip for further analysis. The viability of cells and their inflammatory responses to IL-1β stimulation was investigated. Such a technique would be useful to culture cells in a conventional fashion, which is more convenient and faster, and stimulate cells in an advanced model with perfusion when needed.

scholarly journals Overproduction of growth differentiation factor 15 promotes human rhinovirus infection and virus-induced inflammation in the lung

2018 ◽  
Vol 314 (3) ◽  
pp. L514-L527 ◽  
Author(s):  
Qun Wu ◽  
Di Jiang ◽  
Niccolette R. Schaefer ◽  
Laura Harmacek ◽  
Brian P. O’Connor ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Responses ◽  
Airway Epithelial Cells ◽  
Human Rhinovirus ◽  
Chronic Obstructive ◽  
Airway Epithelial ◽  
Growth Differentiation Factor 15 ◽  
Human Airway ◽  
Differentiation Factor ◽  
Human Airway Epithelial Cells

Human rhinovirus (HRV) is the most common virus contributing to acute exacerbations of chronic obstructive pulmonary disease (COPD) nearly year round, but the mechanisms have not been well elucidated. Recent clinical studies suggest that high levels of growth differentiation factor 15 (GDF15) protein in the blood are associated with an increased yearly rate of all-cause COPD exacerbations. Therefore, in the current study, we investigated whether GDF15 promotes HRV infection and virus-induced lung inflammation. We first examined the role of GDF15 in regulating host defense and HRV-induced inflammation using human GDF15 transgenic mice and cultured human GDF15 transgenic mouse tracheal epithelial cells. Next, we determined the effect of GDF15 on viral replication, antiviral responses, and inflammation in human airway epithelial cells with GDF15 knockdown and HRV infection. Finally, we explored the signaling pathways involved in airway epithelial responses to HRV infection in the context of GDF15. Human GDF15 protein overexpression in mice led to exaggerated inflammatory responses to HRV, increased infectious particle release, and decreased IFN-λ2/3 (IL-28A/B) mRNA expression in the lung. Moreover, GDF15 facilitated HRV replication and inflammation via inhibiting IFN-λ1/IL-29 protein production in human airway epithelial cells. Lastly, Smad1 cooperated with interferon regulatory factor 7 (IRF7) to regulate airway epithelial responses to HRV infection partly via GDF15 signaling. Our results reveal a novel function of GDF15 in promoting lung HRV infection and virus-induced inflammation, which may be a new mechanism for the increased susceptibility and severity of respiratory viral (i.e., HRV) infection in cigarette smoke-exposed airways with GDF15 overproduction.

Innate Inflammatory Responses of Pediatric Cystic Fibrosis Airway Epithelial Cells

2011 ◽  
Vol 44 (6) ◽  
pp. 761-767 ◽  
Author(s):  
Erika N. Sutanto ◽  
Anthony Kicic ◽  
Clara J. Foo ◽  
Paul T. Stevens ◽  
David Mullane ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Epithelial Cells ◽  
Inflammatory Responses ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Cystic Fibrosis Airway

scholarly journals Streamer discharge reduces pollen-induced inflammatory responses and injury in human airway epithelial cells

2013 ◽  
Vol 238 (2) ◽  
pp. 187-192
Author(s):  
Akiko Honda ◽  
Rumiko Murayama ◽  
Kenshi Tsuji ◽  
Yugo Matsuda ◽  
Eiko Koike ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Responses ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Streamer Discharge ◽  
Human Airway ◽  
Human Airway Epithelial Cells

scholarly journals Cultured Human Airway Epithelial Cells (Calu-3): A Model of Human Respiratory Function, Structure, and Inflammatory Responses

2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Yan Zhu ◽  
Aaron Chidekel ◽  
Thomas H. Shaffer
Keyword(s):  
Epithelial Cells ◽  
Cellular Response ◽  
Inflammatory Responses ◽  
Airway Epithelial Cells ◽  
Treatment Modalities ◽  
Positive Pressure ◽  
Dependent Manner ◽  
Airway Epithelial ◽  
Human Airway ◽  
Human Airway Epithelial Cells

This article reviews the application of the human airway Calu-3 cell line as a respiratory model for studying the effects of gas concentrations, exposure time, biophysical stress, and biological agents on human airway epithelial cells. Calu-3 cells are grown to confluence at an air-liquid interface on permeable supports. To model human respiratory conditions and treatment modalities, monolayers are placed in an environmental chamber, and exposed to specific levels of oxygen or other therapeutic modalities such as positive pressure and medications to assess the effect of interventions on inflammatory mediators, immunologic proteins, and antibacterial outcomes. Monolayer integrity and permeability and cell histology and viability also measure cellular response to therapeutic interventions. Calu-3 cells exposed to graded oxygen concentrations demonstrate cell dysfunction and inflammation in a dose-dependent manner. Modeling positive airway pressure reveals that pressure may exert a greater injurious effect and cytokine response than oxygen. In experiments with pharmacological agents, Lucinactant is protective of Calu-3 cells compared with Beractant and control, and perfluorocarbons also protect against hyperoxia-induced airway epithelial cell injury. The Calu-3 cell preparation is a sensitive and efficient preclinical model to study human respiratory processes and diseases related to oxygen- and ventilator-induced lung injury.

scholarly journals Silica Nanoparticles Inhibit ATP Responses of Human Airway Epithelial 16HBE Cells

2021 ◽  
Author(s):  
Alina Milici ◽  
Alicia Sanchez ◽  
Karel Talavera
Keyword(s):  
Silica Nanoparticles ◽  
Mucociliary Clearance ◽  
Inflammatory Responses ◽  
Low Cost ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Bronchial Epithelial ◽  
Molecular Pattern ◽  
Competitive Mechanism ◽  
Exposure Levels

Because of their low cost and easy production silica nanoparticles (NPs) are amply used in multiple manufactures as anti-caking, densifying and hydrophobic agents. However, this has increased the exposure levels of the general population and has raised concerns about possible toxicity of this nanomaterial. NPs are known to affect the function of the airway epithelium, but the biochemical pathways targeted by these particles remain largely unknown. Here we investigated the effects of NPs on the responses of cultured human bronchial epithelial (16HBE) cells to the damage-associated molecular pattern ATP, using fluorometric measurements of intracellular Ca2+ concentration. Upon stimulation with extracellular ATP these cells displayed a concentration-dependent increase in intracellular Ca2+, which was mediated by release from intracellular stores. Silica NPs inhibited the Ca2+ responses to ATP within minutes of application and at low micromolar concentrations, which are significantly faster and more potent than those previously reported for the induction of cellular toxicity and pro-inflammatory responses. NPs-induced inhibition appeared to be independent from the increase in intracellular Ca2+ they produce, and via a non-competitive mechanism. These findings suggest that NPs reduce the ability of airway epithelial cells to mount ATP-dependent protective responses such as the increase in mucociliary clearance and cough.

Oxysophocarpine protects airway epithelial cells against inflammation and apoptosis by inhibiting miR-155 expression

2020 ◽  
Vol 12 (16) ◽  
pp. 1475-1487
Author(s):  
Linfu Li ◽  
Renbing Shi ◽  
Weimei Shi ◽  
Rui Zhang ◽  
Longhuo Wu
Keyword(s):  
Epithelial Cells ◽  
Protein Interactions ◽  
Inflammatory Responses ◽  
Annexin V ◽  
Airway Epithelial Cells ◽  
Protective Effects ◽  
Airway Epithelial ◽  
Quantitative Real Time Pcr ◽  
Protein Expressions ◽  
Anti Inflammation

Oxysophocarpine (OSC) has been documented for anti-inflammatory activity. However, the mechanisms of OSC in anti-inflammation are unclear. Aim: To investigate the protective effects of OSC on inflammation and apoptosis induced by lipopolysaccharide in NCI-H292 and human primary airway epithelial cells. Materials & methods: MTT and Annexin V-FITC/PI staining were used to detect cells viability. Inflammatory responses were determined by ELISA. The quantitative real-time PCR (qRT-PCR) and western blot were used to detect mRNA/miRNA and protein expressions respectively. Co-immunoprecipitation was investigated for protein interactions. Results & conclusion: miR-155 mimics significantly induced cell apoptosis, inflammatory responses and MAPK and NF-κB pathways. NDFIP1 was identified as the target of miR-155. OSC protected cells against apoptosis and inflammatory responses and compromised miR-155 activity by attenuating MAPK and NF-κB pathways.

Obese Adipose Tissue Modulates Pro-inflammatory Responses of Mouse Airway Epithelial Cells

2021 ◽  
Author(s):  
Jennifer L Ather ◽  
Katherine E Van Der Vliet ◽  
Madeleine M Mank ◽  
Leah F Reed ◽  
Anne E Dixon ◽  
...  
Keyword(s):  
Weight Loss ◽  
Epithelial Cells ◽  
High Fat Diet ◽  
Inflammatory Responses ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Obese Mice ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet

Although recognized as an important endocrine organ, little is known about the mechanisms through which adipose tissue can regulate inflammatory responses in distant tissues, such as lung, that are affected by obesity. To explore potential mechanisms, male C57BL/6J mice were provided either high-fat diet, low-fat diet, or were provided a high-fat diet then switched to the low-fat diet to promote weight loss. Visceral adipocytes were then cultured in vitro to generate conditioned media (CM) that was used to treat both primary (MTEC) and immortalized (MTCC) airway epithelial cells. Adiponectin levels were greatly depressed in the CM from both obese and diet-switched adipocytes relative to mice continually fed the low-fat diet. MTEC from obese mice secreted higher baseline levels of inflammatory cytokines than MTEC from lean or diet-switched mice. MTEC treated with obese adipocyte CM increased their secretion of these cytokines compared to MTEC treated with lean CM. Diet-switched CM modestly decreased the production of cytokines compared to obese CM, and these effects were recapitulated when the CM was used to treat MTCC. Adipose stromal vascular cells from obese mice expressed genes consistent with an M1 macrophage phenotype and decreased eosinophil abundance compared to lean SVF, a profile that persisted in the lean diet-switched mice despite substantial weight loss. Soluble factors secreted from obese adipocytes exert a pro-inflammatory effect on airway epithelial cells, and these alterations are attenuated by diet-induced weight loss, which could have implications for the airway dysfunction related to obese asthma and its mitigation by weight loss.

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