scholarly journals Study Effects of Drug Treatment and Physiological Physical Stimulation on Surfactant Protein Expression of Lung Epithelial Cells Using a Biomimetic Microfluidic Cell Culture Device

Micromachines ◽  
2019 ◽  
Vol 10 (6) ◽  
pp. 400 ◽  
Author(s):  
Ting-Ru Lin ◽  
Sih-Ling Yeh ◽  
Chien-Chung Peng ◽  
Wei-Hao Liao ◽  
Yi-Chung Tung
Keyword(s):  
Cell Culture ◽  
Epithelial Cells ◽  
Drug Treatment ◽  
Surfactant Protein ◽  
Lung Epithelial Cells ◽  
Single Chip ◽  
Physical Stimulation ◽  
Lung Epithelial

This paper reports a biomimetic microfluidic device capable of reconstituting physiological physical microenvironments in lungs during fetal development for cell culture. The device integrates controllability of both hydrostatic pressure and cyclic substrate deformation within a single chip to better mimic the in vivo microenvironments. For demonstration, the effects of drug treatment and physical stimulations on surfactant protein C (SPC) expression of lung epithelial cells (A549) are studied using the device. The experimental results confirm the device’s capability of mimicking in vivo microenvironments with multiple physical stimulations for cell culture applications. Furthermore, the results indicate the critical roles of physical stimulations in regulating cellular behaviors. With the demonstrated functionalities and performance, the device is expected to provide a powerful tool for further lung development studies that can be translated to clinical observation in a more straightforward manner. Consequently, the device is promising for construction of more in vitro physiological microenvironments integrating multiple physical stimulations to better study organ development and its functions.

scholarly journals Influenza A Virus Infection Induces Apical Redistribution of Na+, K+-ATPase in Lung Epithelial Cells In Vitro and In Vivo

2019 ◽  
Vol 61 (3) ◽  
pp. 395-398
Author(s):  
Christin Peteranderl ◽  
Irina Kuznetsova ◽  
Jessica Schulze ◽  
Martin Hardt ◽  
Emilia Lecuona ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Virus Infection ◽  
Influenza A Virus ◽  
Influenza A ◽  
Lung Epithelial Cells ◽  
Lung Epithelial ◽  
Influenza A Virus Infection

Maresin 1 Maintains the Permeability of Lung Epithelial Cells In Vitro and In Vivo

Inflammation ◽  
2016 ◽  
Vol 39 (6) ◽  
pp. 1981-1989 ◽  
Author(s):  
Lin Chen ◽  
Hong Liu ◽  
Yaxin Wang ◽  
Haifa Xia ◽  
Jie Gong ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Lung Epithelial ◽  
Maresin 1

scholarly journals Bactofection of lung epithelial cells in vitro and in vivo using a genetically modified Escherichia coli

Gene Therapy ◽  
2008 ◽  
Vol 15 (6) ◽  
pp. 434-442 ◽  
Author(s):  
M D B Larsen ◽  
U Griesenbach ◽  
S Goussard ◽  
D C Gruenert ◽  
D M Geddes ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Genetically Modified ◽  
Lung Epithelial Cells ◽  
Lung Epithelial

Ontogeny of surfactant proteins and lipid-synthesizing enzymes in cultured fetal lung epithelial cells

1994 ◽  
Vol 267 (4) ◽  
pp. L375-L383 ◽  
Author(s):  
C. Fraslon-Vanhulle ◽  
B. Chailley-Heu ◽  
J. J. Batenburg ◽  
R. Elfring ◽  
J. R. Bourbon
Keyword(s):  
Epithelial Cells ◽  
Phospholipid Composition ◽  
Lipid Synthesis ◽  
Fetal Lung ◽  
Surfactant Protein ◽  
Lung Epithelial Cells ◽  
Type Ii Cells ◽  
Type Ii ◽  
Lung Epithelial

Fetal rat lung epithelial cells were isolated on gestational day 17 (term is 22), separated from fibroblasts, and cultured up to 6 days in a serum-free medium on a basement membrane matrix. Surfactant protein (SP) A, barely detectable by immunostaining at the beginning of the culture, considerably increased in cells and subsequently in the lumen of the epithelial cell clusters. SP-A mRNA, already detectable at culture initiation, progressively increased. By contrast, SP-B and its mRNA appeared after 2-3 days. SP-C mRNA appeared only after 4 days of culture. Cells cultured 6 days had a phospholipid composition similar to that of freshly isolated adult rat type II cells. The enhancement of lipid synthesis between the first and the sixth culture days, reported earlier to occur in these cells, was found to be accompanied by a two- to fivefold increase in amount of mRNAs of lipogenic enzymes and choline phosphate cytidylyltransferase. In conclusion, alveolar epithelial type II cells appear to be capable of full differentiation in vitro, and components of the surfactant system are all regulated developmentally at a pretranslational level.

scholarly journals ExGen 500 is an efficient vector for gene delivery to lung epithelial cells in vitro and in vivo

Gene Therapy ◽  
1997 ◽  
Vol 4 (10) ◽  
pp. 1100-1106 ◽  
Author(s):  
S Ferrari ◽  
E Moro ◽  
A Pettenazzo ◽  
JP Behr ◽  
F Zacchello ◽  
...  
Keyword(s):  
Gene Delivery ◽  
Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Lung Epithelial ◽  
Efficient Vector

scholarly journals Antigen presentation by lung epithelial cells directs CD4+ TRM cell function and regulates barrier immunity

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Anukul T. Shenoy ◽  
Carolina Lyon De Ana ◽  
Emad I. Arafa ◽  
Isabelle Salwig ◽  
Kimberly A. Barker ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Antigen Presentation ◽  
Cell Function ◽  
Surface Expression ◽  
Surfactant Protein ◽  
Lung Epithelial Cells ◽  
Mhc Ii ◽  
Lung Epithelial ◽  
Barrier Immunity

AbstractBarrier tissues are populated by functionally plastic CD4+ resident memory T (TRM) cells. Whether the barrier epithelium regulates CD4+ TRM cell locations, plasticity and activities remains unclear. Here we report that lung epithelial cells, including distinct surfactant protein C (SPC)lowMHChigh epithelial cells, function as anatomically-segregated and temporally-dynamic antigen presenting cells. In vivo ablation of lung epithelial MHC-II results in altered localization of CD4+ TRM cells. Recurrent encounters with cognate antigen in the absence of epithelial MHC-II leads CD4+ TRM cells to co-express several classically antagonistic lineage-defining transcription factors, changes their cytokine profiles, and results in dysregulated barrier immunity. In addition, lung epithelial MHC-II is needed for surface expression of PD-L1, which engages its ligand PD-1 to constrain lung CD4+ TRM cell phenotypes. Thus, we establish epithelial antigen presentation as a critical regulator of CD4+ TRM cell function and identify epithelial-CD4+ TRM cell immune interactions as core elements of barrier immunity.

scholarly journals In Vivo Demonstration and Quantification of Intracellular Bacillus anthracis in Lung Epithelial Cells

2008 ◽  
Vol 76 (9) ◽  
pp. 3975-3983 ◽  
Author(s):  
Brooke H. Russell ◽  
Qing Liu ◽  
Sarah A. Jenkins ◽  
Michael J. Tuvim ◽  
Burton F. Dickey ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Bacillus Anthracis ◽  
Intracellular Localization ◽  
Lung Epithelial Cells ◽  
Early Event ◽  
Thin Sections ◽  
Isolated Lung ◽  
Lung Epithelial

ABSTRACT Inhalational anthrax is initiated by the entry of Bacillus anthracis spores into the lung. A critical early event in the establishment of an infection is the dissemination of spores from the lung. Using in vitro cell culture assays, we previously demonstrated that B. anthracis spores are capable of entering into epithelial cells of the lung and crossing a barrier of lung epithelial cells without apparent disruption of the barrier integrity, suggesting a novel portal for spores to disseminate from the lung. However, in vivo evidence for spore uptake by epithelial cells has been lacking. Here, using a mouse model, we present evidence that B. anthracis spores are taken up by lung epithelial cells in vivo soon after spores are delivered into the lung. Immunofluorescence staining of thin sections of lungs from spore-challenged BALB/c mice revealed that spores were associated with the epithelial surfaces in the airway and the alveoli at 2 and 4 h postinoculation. Confocal analysis further indicated that some of the associated spores were surrounded by F-actin, demonstrating intracellular localization. These observations were further confirmed and substantiated by a quantitative method that first isolated lung cells from spore-challenged mice and then stained these cells with antibodies specific for epithelial cells and spores. The results showed that substantial amounts of spores were taken up by lung epithelial cells in vivo. These data, combined with those in our previous reports, provided powerful evidence that the lung epithelia were directly targeted by B. anthracis spores at early stages of infection.

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