Transmigration of Leukocytes Across Epithelial Monolayers

2018 ◽  
pp. 59-70
Author(s):  
Penny E. Morton ◽  
Maddy Parsons
Keyword(s):  
Epithelial Monolayers

Formation of epithelial monolayers and acinotubular complexes from rat and human salivary origin

Pancreatology ◽  
2014 ◽  
Vol 14 (3) ◽  
pp. S121
Author(s):  
Gabor Varga ◽  
Erzsebet Bori ◽  
Orsolya Hegyesi ◽  
Irma Demeter ◽  
Beata Burghardt ◽  
...  
Keyword(s):  
Epithelial Monolayers

Nonmitogenic morphoregulatory action of pp60v-src on multicellular epithelial structures

1987 ◽  
Vol 7 (4) ◽  
pp. 1326-1337
Author(s):  
S L Warren ◽  
W J Nelson
Keyword(s):  
Tyrosine Kinases ◽  
Mdck Cells ◽  
Growth Potential ◽  
Junctional Complex ◽  
Madin Darby Canine Kidney ◽  
Epithelial Monolayers ◽  
Zonula Occludens ◽  
Darby Canine Kidney ◽  
Canine Kidney

Madin-Darby canine kidney (MDCK) cells form polarized, multicellular epithelial structures in vitro. Low-level expression of pp60v-src in MDCK cells elicits plasticity in these multicellular structures. Plasticity was revealed by the displacement of cells from mechanically stressed regions of the epithelial monolayers; however, the two-dimensional relationship between the cells in the remainder of the monolayer was maintained. Electron microscopy of multicellular structures revealed abnormal separation of the lateral membranes of adjacent cells and selective uncoupling of the junctional complex; the zonula adherens was disrupted, but the zonula occludens and desmosomes were retained. Significantly, this result was not accompanied by transformation of the cells, as judged by the absence of anchorage-independent growth potential. These results demonstrate a nonmitogenic biological activity of pp60v-src which is experimentally dissociable from transformation. This morphoregulatory action on higher-order epithelial structures may reflect a function of related cellular tyrosine kinases.

scholarly journals Effects of the Immunoglobulin A1 Protease on Neisseria gonorrhoeae Trafficking across Polarized T84 Epithelial Monolayers

2000 ◽  
Vol 68 (2) ◽  
pp. 906-911 ◽  
Author(s):  
Sylvia Hopper ◽  
Brandi Vasquez ◽  
Alex Merz ◽  
Susan Clary ◽  
J. Scott Wilbur ◽  
...  
Keyword(s):  
Neisseria Gonorrhoeae ◽  
Solid Substrate ◽  
Carcinoma Cells ◽  
Wild Type ◽  
Epithelial Monolayers ◽  
Iga1 Protease ◽  
Epithelial Barriers ◽  
Type Strains ◽  
Mediated Reduction ◽  
Human Epidermoid Carcinoma

ABSTRACT We previously demonstrated that the Neisseria IgA1 protease cleaves LAMP1 (lysosome-associated membrane protein 1), a major integral membrane glycoprotein of lysosomes, thereby accelerating its degradation rate in infected A431 human epidermoid carcinoma cells and resulting in the alteration of lysosomes in these cells. In this study, we determined whether the IgA1 protease also affects the trafficking of Neisseria gonorrhoeae across polarized T84 epithelial monolayers. We report that N. gonorrhoeaeinfection of T84 monolayers, grown on a solid substrate or polarized on semiporous membranes, also results in IgA1 protease-mediated reduction of LAMP1. We demonstrate that iga mutants in two genetic backgrounds exited polarized T84 monolayers in fewer numbers than the corresponding wild-type strains. Finally, we present evidence that these mutants have a statistically significant and reproducible defect in their ability to traverse T84 monolayers. These results add to our previous data by showing that the IgA1 protease alters lysosomal content in polarized as well as unpolarized cells and by demonstrating a role for the protease in the traversal of epithelial barriers by N. gonorrhoeae.

scholarly journals Cytochalasin B modulation of Caco-2 tight junction barrier: role of myosin light chain kinase

2000 ◽  
Vol 279 (5) ◽  
pp. G875-G885 ◽  
Author(s):  
Thomas Y. Ma ◽  
Neil T. Hoa ◽  
Daniel D. Tran ◽  
Vuong Bui ◽  
Ali Pedram ◽  
...  
Keyword(s):  
Tight Junction ◽  
Light Chain ◽  
Myosin Light Chain Kinase ◽  
Myosin Light Chain ◽  
Cytochalasin B ◽  
Late Phase ◽  
Metabolic Inhibitors ◽  
Intestinal Epithelial ◽  
Atpase Inhibitor ◽  
Epithelial Monolayers

The intracellular mechanisms that mediate cytochalasin-induced increase in intestinal epithelial tight junction (TJ) permeability are unclear. In this study, we examined the involvement of myosin light chain kinase (MLCK) in this process, using the filter-grown Caco-2 intestinal epithelial monolayers. Cytochalasin B (Cyto B) (5 μg/ml) produced an increase in Caco-2 MLCK activity, which correlated with the increase in Caco-2 TJ permeability. The inhibition of Cyto B-induced MLCK activation prevented the increase in Caco-2 TJ permeability. Additionally, myosin-Mg2+-ATPase inhibitor and metabolic inhibitors (which inhibit MLCK induced actin-myosin contraction) also prevented the Cyto B-induced increase in Caco-2 TJ permeability. Cyto B caused a late-phase (15–30 min) aggregation of actin fragments into large actin clumps, which was also inhibited by MLCK inhibitors. Cyto B produced a morphological disturbance of the ZO-1 TJ proteins, visually correlating with the functional increase in Caco-2 TJ permeability. The MLCK and myosin-Mg2+-ATPase inhibitors prevented both the functional increase in TJ permeability and disruption of ZO-1 proteins. These findings suggested that Cyto B-induced increase in Caco-2 TJ permeability is regulated by MLCK activation.

scholarly journals Targeted replacement of full-length CFTR in human airway stem cells by CRISPR/Cas9 for pan-mutation correction in the endogenous locus

2021 ◽  
Author(s):  
Sriram Vaidyanathan ◽  
Ron Baik ◽  
Lu Chen ◽  
Dawn T. Bravo ◽  
Carlos J. Suarez ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Stem Cells ◽  
Upper Airway ◽  
Pathogenic Mutation ◽  
Monogenic Disease ◽  
Transmembrane Conductance Regulator ◽  
Epithelial Monolayers ◽  
Cftr Protein ◽  
Almost All ◽  
Air Liquid Interface

AbstractCystic fibrosis (CF) is a monogenic disease caused by impaired production and/or function of the cystic fibrosis transmembrane conductance regulator (CFTR) protein. Although we have previously shown correction of the most common pathogenic mutation, there are many other pathogenic mutations throughout the CF gene. An autologous airway stem cell therapy in which the CFTR cDNA is precisely inserted into the CFTR locus may enable the development of a durable cure for almost all CF patients, irrespective of the causal mutation. Here, we use CRISPR/Cas9 and two adeno-associated viruses (AAV) carrying the two halves of the CFTR cDNA to sequentially insert the full CFTR cDNA along with a truncated CD19 (tCD19) enrichment tag in upper airway basal stem cells (UABCs) and human bronchial basal stem cells (HBECs). The modified cells were enriched to obtain 60-80% tCD19+ UABCs and HBECs from 11 different CF donors with a variety of mutations. Differentiated epithelial monolayers cultured at air-liquid interface showed restored CFTR function that was >70% of the CFTR function in non-CF controls. Thus, our study enables the development of a therapy for almost all CF patients, including patients who cannot be treated using recently approved modulator therapies.

scholarly journals Active morphogenesis of epithelial monolayers

2019 ◽  
Vol 100 (2) ◽  
Author(s):  
Richard G. Morris ◽  
Madan Rao
Keyword(s):  
Epithelial Monolayers

Regulation of pepsinogen release from canine chief cells in primary monolayer culture

1983 ◽  
Vol 245 (5) ◽  
pp. G641-G646 ◽  
Author(s):  
M. J. Sanders ◽  
D. A. Amirian ◽  
A. Ayalon ◽  
A. H. Soll
Keyword(s):  
Phosphodiesterase Inhibitor ◽  
Functional Differentiation ◽  
Maximal Response ◽  
Chief Cells ◽  
Epithelial Monolayers ◽  
Pepsinogen Secretion ◽  
Primary Monolayer ◽  
Dose Dependent ◽  
Short Term Culture ◽  
Stimulation Of

To study the regulation of pepsinogen secretion by chief cells, we have developed techniques for the isolation, enrichment, and short-term culture of chief cells from canine stomach. The fundic mucosa was enzyme dispersed and chief cells were enriched to a content of about 70% using an elutriator rotor. After 36 h in culture confluent monolayers formed that were highly enriched in chief cells. Carbachol induced a time-dependent release of pepsinogen into the medium, with about a threefold increase in pepsinogen secretion over controls found after 60 min of incubation. Carbachol stimulation of pepsinogen secretion was dose dependent, with 5 microM producing 50% of the maximal response found at a carbachol concentration of 100 microM. Atropine (100 microM) produced a rightward shift of the dose-response curve, indicating the presence of a muscarinic receptor. Dibutyryl cAMP, 8-bromo-cAMP, and forskolin also markedly stimulated pepsinogen secretion. Secretin and vasoactive intestinal peptide (VIP) stimulated pepsinogen secretion, but the response were of smaller magnitude than found with carbachol or the cAMP analogues. The phosphodiesterase inhibitor isobutylmethylxanthine also caused a small stimulation of pepsinogen secretion but did not enhance the response to secretin or VIP. These findings indicate that epithelial monolayers can spontaneously form from isolated canine chief cells and retain functional differentiation evident by a response to stimulation. Canine chief cells in culture possess muscarinic and secretin receptors and respond to cAMP.

scholarly journals Hydrodynamic instabilities, waves and turbulence in spreading epithelia

Soft Matter ◽  
2017 ◽  
Vol 13 (38) ◽  
pp. 6913-6928 ◽  
Author(s):  
C. Blanch-Mercader ◽  
J. Casademunt
Keyword(s):  
Hydrodynamic Model ◽  
Viscous Fluids ◽  
Hydrodynamic Instabilities ◽  
Comprehensive Understanding ◽  
Collective Dynamics ◽  
Epithelial Monolayers

We present a hydrodynamic model of spreading epithelial monolayers described as polar viscous fluids, with active contractility and tractions. Our model provides a comprehensive understanding of a variety of observations and makes simple predictions to further test their collective dynamics.

scholarly journals Nonmitogenic morphoregulatory action of pp60v-src on multicellular epithelial structures.

1987 ◽  
Vol 7 (4) ◽  
pp. 1326-1337 ◽  
Author(s):  
S L Warren ◽  
W J Nelson
Keyword(s):  
Tyrosine Kinases ◽  
Mdck Cells ◽  
Growth Potential ◽  
Junctional Complex ◽  
Madin Darby Canine Kidney ◽  
Epithelial Monolayers ◽  
Zonula Occludens ◽  
Darby Canine Kidney ◽  
Canine Kidney

Madin-Darby canine kidney (MDCK) cells form polarized, multicellular epithelial structures in vitro. Low-level expression of pp60v-src in MDCK cells elicits plasticity in these multicellular structures. Plasticity was revealed by the displacement of cells from mechanically stressed regions of the epithelial monolayers; however, the two-dimensional relationship between the cells in the remainder of the monolayer was maintained. Electron microscopy of multicellular structures revealed abnormal separation of the lateral membranes of adjacent cells and selective uncoupling of the junctional complex; the zonula adherens was disrupted, but the zonula occludens and desmosomes were retained. Significantly, this result was not accompanied by transformation of the cells, as judged by the absence of anchorage-independent growth potential. These results demonstrate a nonmitogenic biological activity of pp60v-src which is experimentally dissociable from transformation. This morphoregulatory action on higher-order epithelial structures may reflect a function of related cellular tyrosine kinases.

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