Lactosylated polyethylenimine for gene transfer into airway epithelial cells: role of the sugar moiety in cell delivery and intracellular trafficking of the complexes

2004 ◽  
Vol 6 (3) ◽  
pp. 345-356 ◽  
Author(s):  
Stéphanie Grosse ◽  
Yolande Aron ◽  
Isabelle Honoré ◽  
Guiti Thévenot ◽  
Claire Danel ◽  
...  
Keyword(s):  
Gene Transfer ◽  
Epithelial Cells ◽  
Intracellular Trafficking ◽  
Airway Epithelial Cells ◽  
Cell Delivery ◽  
Airway Epithelial ◽  
Sugar Moiety

Role of size and composition of traffic and agricultural aerosols in the molecular responses triggered in airway epithelial cells

2011 ◽  
Vol 23 (11) ◽  
pp. 627-640 ◽  
Author(s):  
Val Stéphanie ◽  
Martinon Laurent ◽  
Cachier Hélène ◽  
Yahyaoui Abderrazak ◽  
Marfaing Hélène ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Molecular Responses

Uptake of plasmid/glycosylated polymer complexes and gene transfer efficiency in differentiated airway epithelial cells

2002 ◽  
Vol 5 (1) ◽  
pp. 38-48 ◽  
Author(s):  
Isabelle Fajac ◽  
Guiti Thévenot ◽  
Laurent Bédouet ◽  
Claire Danel ◽  
Marc Riquet ◽  
...  
Keyword(s):  
Gene Transfer ◽  
Epithelial Cells ◽  
Airway Epithelial Cells ◽  
Transfer Efficiency ◽  
Airway Epithelial ◽  
Polymer Complexes ◽  
Gene Transfer Efficiency

scholarly journals Protective role of Indoleamine 2,3 dioxygenase in Respiratory Syncytial Virus associated immune response in airway epithelial cells

Virology ◽  
2017 ◽  
Vol 512 ◽  
pp. 144-150 ◽  
Author(s):  
Devi Rajan ◽  
Raghavan Chinnadurai ◽  
Evan L. O'Keefe ◽  
Seyhan Boyoglu-Barnum ◽  
Sean O. Todd ◽  
...  
Keyword(s):  
Immune Response ◽  
Respiratory Syncytial Virus ◽  
Epithelial Cells ◽  
Protective Role ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Indoleamine 2,3 Dioxygenase ◽  
Syncytial Virus

Airway epithelial tight junctions and binding and cytotoxicity ofPseudomonas aeruginosa

1999 ◽  
Vol 277 (1) ◽  
pp. L204-L217 ◽  
Author(s):  
Alfred Lee ◽  
Dar Chow ◽  
Brian Haus ◽  
Wanru Tseng ◽  
David Evans ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Tight Junctions ◽  
Propidium Iodide ◽  
Time Course ◽  
Living Cells ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Basolateral Membranes ◽  
Free Edges

The role of tight junctions in the binding and cytoxicity of Pseudomonas aeruginosato apical or basolateral membranes of lung airway epithelial cells was tested with fluorescence microscopy on living cells. Binding of noncytotoxic P. aeruginosa strain O1 was assessed with P. aeruginosa that expressed green fluorescent protein. Binding of cytotoxic P. aeruginosa strain 6206 was assessed with FITC-labeled P. aeruginosa; cytotoxicity was determined from nuclear uptake of the impermeant dye propidium iodide. The role of direct contact of P. aeruginosa to epithelial cells was tested with filters with small (0.45-μm) or large (2.0-μm) pores. High transepithelial resistance ( Rt) Calu-3 and cultured bovine tracheal monolayers ( Rt> 1,000 Ω ⋅ cm2) bound P. aeruginosa very infrequently (<1 P. aeruginosa/100 cells) at the apical membrane, but P. aeruginosabound frequently to cells near “free edges” at holes, wounds, islands, and perimeters; cytotoxicity required direct interaction with basolateral membranes. Wounded high Rtepithelia showed increased P. aeruginosa binding and cytotoxicity at the free edges because basolateral membranes were accessible to P. aeruginosa, and dead and living cells near the wound bound P. aeruginosa similarly. Compared with high Rtepithelia, low RtCFT1 ( Rt= 100–200 Ω ⋅ cm2) and EGTA-treated Calu-3 monolayers were 25 times more susceptible to P. aeruginosa binding throughout the monolayer. Cytotoxicity to CFT1 cells (throughout the confluent monolayer, not only at the free edge) occurred after a shorter delay (0.25 vs. 2.0 h) and then five times faster than to Calu-3 cells, indicating that the time course of P. aeruginosa cytotoxicity may be limited by the rate of gaining access through tight junctions and that this occurred faster in low Rtthan in high Rtairway epithelia. Cytotoxicity appeared to occur in a sequential process that led first to a loss of fura 2 and a later uptake of propidium iodide. P. aeruginosa bound three times more frequently to regions between cells (tight junctions?) than to cell membranes of low RtCFT1 cells.

scholarly journals Role of retinoic acid inducible gene-I in human metapneumovirus-induced cellular signalling

2008 ◽  
Vol 89 (8) ◽  
pp. 1978-1986 ◽  
Author(s):  
S. Liao ◽  
X. Bao ◽  
T. Liu ◽  
S. Lai ◽  
K. Li ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Epithelial Cells ◽  
Gene Transcription ◽  
Airway Epithelial Cells ◽  
Human Metapneumovirus ◽  
Airway Epithelial ◽  
Cellular Signalling ◽  
Hmpv Infection ◽  
Inducible Gene

Human metapneumovirus (HMPV) is a recently discovered pathogen that causes a significant proportion of respiratory infections in young infants, the elderly and immunocompromised patients. Very little is known regarding the cellular signalling elicited by this virus in airway epithelial cells, the target of HMPV infection. In this study, we investigated the role of the RNA helicases retinoic acid inducible gene-I (RIG-I) and melanoma differentiation-associated gene-5 (MDA-5) as the main pattern recognition receptors (PRRs) involved in viral detection and subsequent expression of proinflammatory and antiviral genes. HMPV infection readily induced RIG-I and MDA-5 gene and protein expression in A549 cells, a type II-like alveolar epithelial cell line. Expression of dominant-negative (DN) RIG-I or downregulation of RIG-I gene expression using small interfering RNA (siRNA) significantly decreased HMPV-induced beta interferon (IFN-β), interleukin (IL)-8 and RANTES gene transcription, by inhibiting viral-induced activation of nuclear factor (NF)-κB and interferon regulatory factor (IRF), leading to enhanced viral replication. On the other hand, MDA-5 did not seem to play a significant role in HMPV-induced cellular responses. Mitochondrial antiviral signalling protein (MAVS), an adaptor protein linking both RIG-I and MDA-5 to downstream activation of IRF-3 and NF-κB, was also necessary for HMPV-induced cellular signalling. Expression of a DN MAVS significantly reduced IFN-β and chemokine gene transcription, by inhibiting NF-κB- and IRF-dependent gene transcription, in response to HMPV infection. Our results show that HMPV activates the RIG-I–MAVS signalling pathway in airway epithelial cells, leading to the expression of important proinflammatory and antiviral molecules involved in the innate immune response to viruses.

scholarly journals A Novel Role of Protein Tyrosine Kinase2 in Mediating Chloride Secretion in Human Airway Epithelial Cells

PLoS ONE ◽  
2011 ◽  
Vol 6 (7) ◽  
pp. e21991 ◽  
Author(s):  
Lihua Liang ◽  
Owen M. Woodward ◽  
Zhaohui Chen ◽  
Robert Cotter ◽  
William B. Guggino
Keyword(s):  
Epithelial Cells ◽  
Chloride Secretion ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Protein Tyrosine ◽  
Human Airway ◽  
Human Airway Epithelial Cells

scholarly journals Agonist‐stimulated calcium decreases in ovine ciliated airway epithelial cells: role of mitochondria

2001 ◽  
Vol 531 (1) ◽  
pp. 13-26 ◽  
Author(s):  
Matthias Salathe ◽  
Pedro I. Ivonnet ◽  
Thomas Lieb ◽  
Richard J. Bookman
Keyword(s):  
Epithelial Cells ◽  
Airway Epithelial Cells ◽  
Airway Epithelial
Sign in / Sign up

Export Citation Format

Share Document