Invasion of Epithelial Cell Monolayers by Turkey Strains of Pasteurella multocida

1994 ◽  
Vol 38 (1) ◽  
pp. 72 ◽  
Author(s):  
Margie D. Lee ◽  
Richard E. Wooley ◽  
John R. Glisson
Keyword(s):  
Epithelial Cell ◽  
Pasteurella Multocida ◽  
Cell Monolayers ◽  
Epithelial Cell Monolayers

scholarly journals Characteristics of Passive Solute Transport across Primary Rat Alveolar Epithelial Cell Monolayers

Membranes ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 331
Author(s):  
Yong Ho Kim ◽  
Kwang-Jin Kim ◽  
David Z. D’Argenio ◽  
Edward D. Crandall
Keyword(s):  
Epithelial Cell ◽  
Tight Junctions ◽  
Pore Radius ◽  
Alveolar Epithelial Cell ◽  
Alveolar Epithelial Cells ◽  
Type I ◽  
Cell Monolayers ◽  
Alveolar Epithelial ◽  
Epithelial Cell Monolayers ◽  
Hydrophilic Solutes

Primary rat alveolar epithelial cell monolayers (RAECM) were grown without (type I cell-like phenotype, RAECM-I) or with (type II cell-like phenotype, RAECM-II) keratinocyte growth factor to assess passive transport of 11 hydrophilic solutes. We estimated apparent permeability (Papp) in the absence/presence of calcium chelator EGTA to determine the effects of perturbing tight junctions on “equivalent” pores. Papp across RAECM-I and -II in the absence of EGTA are similar and decrease as solute size increases. We modeled Papp of the hydrophilic solutes across RAECM-I/-II as taking place via heterogeneous populations of equivalent pores comprised of small (0.41/0.32 nm radius) and large (9.88/11.56 nm radius) pores, respectively. Total equivalent pore area is dominated by small equivalent pores (99.92–99.97%). The number of small and large equivalent pores in RAECM-I was 8.55 and 1.29 times greater, respectively, than those in RAECM-II. With EGTA, the large pore radius in RAECM-I/-II increased by 1.58/4.34 times and the small equivalent pore radius increased by 1.84/1.90 times, respectively. These results indicate that passive diffusion of hydrophilic solutes across an alveolar epithelium occurs via small and large equivalent pores, reflecting interactions of transmembrane proteins expressed in intercellular tight junctions of alveolar epithelial cells.

scholarly journals A Novel Pharmacological Approach to Enhance the Integrity and Accelerate Restitution of the Intestinal Epithelial Barrier

2020 ◽  
Vol 26 (9) ◽  
pp. 1340-1352
Author(s):  
Xuelei Cao ◽  
Lei Sun ◽  
Susana Lechuga ◽  
Nayden G Naydenov ◽  
Alex Feygin ◽  
...  
Keyword(s):  
Wound Healing ◽  
Epithelial Cell ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Intestinal Epithelial Barrier ◽  
Cell Monolayers ◽  
Barrier Disruption ◽  
Epithelial Cell Monolayers ◽  
Immunofluorescence Labeling ◽  
E Cadherin

Abstract Background Disruption of the gut barrier is an essential mechanism of inflammatory bowel diseases (IBDs) contributing to the development of mucosal inflammation. A hallmark of barrier disruption is the disassembly of epithelial adherens junctions (AJs) driven by decreased expression of a major AJ protein, E-cadherin. A group of isoxazole compounds, such as E-cadherin-upregulator (ECU) and ML327, were previously shown to stimulate E-cadherin expression in poorly differentiated human cancer cells. This study was designed to examine whether these isoxazole compounds can enhance and protect model intestinal epithelial barriers in vitro. Methods The study was conducted using T84, SK-CO15, and HT-29 human colonic epithelial cell monolayers. Disruption of the epithelial barrier was induced by pro-inflammatory cytokines, tumor necrosis factor-α, and interferon-γ. Barrier integrity and epithelial junction assembly was examined using different permeability assays, immunofluorescence labeling, and confocal microscopy. Epithelial restitution was analyzed using a scratch wound healing assay. Results E-cadherin-upregulator and ML327 treatment of intestinal epithelial cell monolayers resulted in several barrier-protective effects, including reduced steady-state epithelial permeability, inhibition of cytokine-induced barrier disruption and junction disassembly, and acceleration of epithelial wound healing. Surprisingly, these effects were not due to upregulation of E-cadherin expression but were mediated by multiple mechanisms including inhibition of junction protein endocytosis, attenuation of cytokine-induced apoptosis, and activation of promigratory Src and AKT signaling. Conclusions Our data highlight ECU and ML327 as promising compounds for developing new therapeutic strategies to protect the integrity and accelerate the restitution of the intestinal epithelial barrier in IBD and other inflammatory disorders.

Mechanisms of liquid flux across pulmonary alveolar epithelial cell monolayers

1997 ◽  
Vol 33 (3) ◽  
pp. 195-200 ◽  
Author(s):  
Gerasimos S. Filippatos ◽  
W. Frank Hughes ◽  
Renli Qiao ◽  
J. Iasha Sznajder ◽  
Bruce D. Uhal
Keyword(s):  
Epithelial Cell ◽  
Alveolar Epithelial Cell ◽  
Cell Monolayers ◽  
Alveolar Epithelial ◽  
Liquid Flux ◽  
Epithelial Cell Monolayers

Characterization of bovine oviduct epithelial cell monolayers cultured under serum-free conditions

1995 ◽  
Vol 31 (9) ◽  
pp. 664-670 ◽  
Author(s):  
A. Van Langendonckt ◽  
A. Vansteenbrugge ◽  
C. Dessy-Doize ◽  
J. E. Flechon ◽  
G. Charpigny ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Serum Free ◽  
Cell Monolayers ◽  
Oviduct Epithelial Cell ◽  
Epithelial Cell Monolayers ◽  
Serum Free Conditions

scholarly journals A Simple Method to Test Mechanical Strain on Epithelial Cell Monolayers Using a 3D-Printed Stretcher

2020 ◽  
Author(s):  
Amanda C. Daulagala ◽  
John Yost ◽  
Amirreza Yeganegi ◽  
William J. Richardson ◽  
Michael J. Yost ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Mechanical Strain ◽  
Simple Method ◽  
Cell Monolayers ◽  
3D Printed ◽  
Epithelial Cell Monolayers

Modulation of ion conductance and active transport by TGF-β1 in alveolar epithelial cell monolayers

2003 ◽  
Vol 285 (6) ◽  
pp. L1192-L1200 ◽  
Author(s):  
Brigham C. Willis ◽  
Kwang-Jin Kim ◽  
Xian Li ◽  
Janice Liebler ◽  
Edward D. Crandall ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Active Transport ◽  
Alveolar Epithelial Cell ◽  
Alveolar Type ◽  
Type I ◽  
Ion Conductance ◽  
Cell Monolayers ◽  
Alveolar Epithelial ◽  
Epithelial Cell Monolayers ◽  
Tgf Β1

Transforming growth factor-β1 (TGF-β1) may be a critical mediator of lung injury and subsequent remodeling during recovery. We evaluated the effects of TGF-β1 on the permeability and active ion transport properties of alveolar epithelial cell monolayers. Rat alveolar type II cells plated on polycarbonate filters in defined serum-free medium form confluent monolayers and acquire the phenotypic characteristics of alveolar type I cells. Exposure to TGF-β1 (0.1-100 pM) from day 0 resulted in a concentration- and time-dependent decrease in transepithelial resistance ( Rt) and increase in short-circuit current ( Isc). Apical amiloride or basolateral ouabain on day 6 inhibited Isc by 80 and 100%, respectively. Concurrent increases in expression of Na+-K+-ATPase α1- and β1-subunits were observed in TGF-β1-treated monolayers. No change in the α-subunit of the rat epithelial sodium channel (α-rENaC) was seen. Exposure of confluent monolayers to TGF-β1 from day 4 resulted in an initial decrease in Rt within 6 h, followed by an increase in Isc over 72-96 h. These results demonstrate that TGF-β1 modulates ion conductance and active transport characteristics of the alveolar epithelium, associated with increased Na+-K+-ATPase, but without a change in α-rENaC.

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