scholarly journals Gonococcal invasion into epithelial cells depends on both cell polarity and ezrin

2021 ◽  
Vol 17 (12) ◽  
pp. e1009592
Author(s):  
Qian Yu ◽  
Liang-Chun Wang ◽  
Sofia Di Benigno ◽  
Daniel C. Stein ◽  
Wenxia Song
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Polarity ◽  
Immunofluorescence Microscopy ◽  
Myosin Ii ◽  
Epithelial Cell Line ◽  
Cervical Tissue ◽  
Polarized Epithelial Cells ◽  
Cervical Epithelial Cells ◽  
Muscle Myosin

Neisseria gonorrhoeae (GC) establishes infection in women from the cervix, lined with heterogeneous epithelial cells from non-polarized stratified at the ectocervix to polarized columnar at the endocervix. We have previously shown that GC differentially colonize and transmigrate across the ecto and endocervical epithelia. However, whether and how GC invade into heterogeneous cervical epithelial cells is unknown. This study examined GC entry of epithelial cells with various properties, using human cervical tissue explant and non-polarized/polarized epithelial cell line models. While adhering to non-polarized and polarized epithelial cells at similar levels, GC invaded into non-polarized more efficiently than polarized epithelial cells. The enhanced GC invasion in non-polarized epithelial cells was associated with increased ezrin phosphorylation, F-actin and ezrin recruitment to GC adherent sites, and the elongation of GC-associated microvilli. Inhibition of ezrin phosphorylation inhibited F-actin and ezrin recruitment and microvilli elongation, leading to a reduction in GC invasion. The reduced GC invasion in polarized epithelial cells was associated with non-muscle myosin II-mediated F-actin disassembly and microvilli denudation at GC adherence sites. Surprisingly, intraepithelial GC were only detected inside epithelial cells shedding from the cervix by immunofluorescence microscopy, but not significantly in the ectocervical and the endocervical regions. We observed similar ezrin and F-actin recruitment in exfoliated cervical epithelial cells but not in those that remained in the ectocervical epithelium, as the luminal layer of ectocervical epithelial cells expressed ten-fold lower levels of ezrin than those beneath. However, GC inoculation induced F-actin reduction and myosin recruitment in the endocervix, similar to what was seen in polarized epithelial cells. Collectively, our results suggest that while GC invade non-polarized epithelial cells through ezrin-driven microvilli elongation, the apical polarization of ezrin and F-actin inhibits GC entry into polarized epithelial cells.

scholarly journals Gonococcal invasion into epithelial cells depends on both cell polarity and ezrin

2021 ◽  
Author(s):  
Qian Yu ◽  
Liang-Chun Wang ◽  
Daniel C. Stein ◽  
Wenxia Song
Keyword(s):  
Epithelial Cells ◽  
Immunofluorescence Microscopy ◽  
Myosin Ii ◽  
Epithelial Cell Line ◽  
Apical Surface ◽  
Cervical Tissue ◽  
Symptomatic Infection ◽  
Polarized Epithelial Cells ◽  
Cervical Epithelial Cells ◽  
Muscle Myosin

AbstractNeisseria gonorrhoeae (GC) establishes symptomatic infection in women from the cervix, lined with heterogeneous epithelial cells from non-polarized stratified at the ectocervix to polarized columnar at the endocervix. We have previously shown that GC differentially colonize and transmigrate across the ecto and endocervical epithelia. However, whether and how GC invade into heterogeneous cervical epithelial cells is unknown. This study examined GC entry of epithelial cells with various properties, using human cervical tissue explant and non-polarized/polarized epithelial cell line models. While adhering to non-polarized and polarized epithelial cells at similar levels, GC invaded into non-polarized more efficiently than polarized epithelial cells. The enhanced GC invasion in non-polarized epithelial cells was associated with increased ezrin phosphorylation, F-actin and ezrin recruitment to GC adherent sites, and the elongation of GC-associated microvilli. Inhibition of ezrin phosphorylation inhibited F-actin and ezrin recruitment and microvilli elongation, leading to a reduction in GC invasion. The reduced GC invasion in polarized epithelial cells was associated with non-muscle myosin II-mediated F-actin disassembly and microvilli ablation at GC adherence sites. Surprisingly, intraepithelial GC were only detected inside epithelial cells shed from the cervix, but neither in the ectocervix nor the endocervix, by immunofluorescence microscopy. We observed similar ezrin and F-actin recruitment in exfoliated cervical epithelial cells but not in those that remained in the ectocervical epithelium, as the luminal layer of ectocervical epithelial cells expressed ten-fold lower levels of ezrin than those beneath. However, GC inoculation induced F-actin reduction and myosin recruitment in the endocervix, similar to what was seen in polarized epithelial cells. Thus, polarized expression of ezrin at the apical surface of epithelial cells inhibits GC invasion, while non-polarized expression of ezrin promotes GC invasion by driving actin accumulation and microvilli elongation.

scholarly journals Move your microvilli

2014 ◽  
Vol 207 (1) ◽  
pp. 9-11 ◽  
Author(s):  
Robert S. Fischer
Keyword(s):  
Wound Healing ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Polarity ◽  
Apical Membrane ◽  
Apical Surface ◽  
Epithelial Cell Polarity ◽  
Cell Biol ◽  
Polarized Epithelial Cells

Polarized epithelial cells create tightly packed arrays of microvilli in their apical membrane, but the fate of these microvilli is relatively unknown when epithelial cell polarity is lost during wound healing. In this issue, Klingner et al. (2014. J. Cell Biol. http://dx.doi.org/10.1083/jcb.201402037) show that, when epithelial cells become subconfluent, actomyosin contractions locally within the apical cortex cause their microvilli to become motile over the dorsal/apical surface. Their unexpected observations may have implications for epithelial responses in wound healing and disease.

scholarly journals A Comparative Study on the Model of PM2.5 Direct or Indirect Interaction with Bronchial Epithelial Cells.

2021 ◽  
Author(s):  
Yan Wang ◽  
Xin Zuo ◽  
Fuyang Jiang ◽  
Lin Hou ◽  
Qiyue Jiang ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Damage ◽  
Direct Interaction ◽  
Bronchial Epithelial Cell ◽  
Human Bronchial Epithelial Cell ◽  
Exposure Model ◽  
Epithelial Cell Line ◽  
Bronchial Epithelial ◽  
The Impact

Abstract The impact of PM2.5 on epithelial cells is a pivotal process leading to many lung pathological changes and pulmonary diseases. In addition to PM2.5 direct interaction with epithelia, macrophages that engulf PM2.5 may also influence the function of epithelial cells. However, among the toxic researches of PM2.5, there is a lack of evaluation of direct or indirect exposure model on human bronchial epithelial cell against PM2.5. In this present research, PM2.5-exposed human bronchial epithelial cell line (BEAS-2B) serves as the direct interaction model, while the contrast is to indirect stimulation model, which takes advantage of transwell co-culture system to carry out that PM2.5 is promptly contacted with macrophages rather than BEAS-2B. By comparing these two modes of interaction, we determined the viability of BEAS-2B and mRNA and/or protein expression profile of transcription factors Nrf2,NF-kB and according inflammatory indicators, with a view to evaluating the effects of different interaction modes of PM2.5 on epithelial cell damage in vitro. We have found that macrophage involvement may protect epithelia from PM2.5 cytotoxic effect, while strengthen the inflammation response.

Studying Permeability in a Commonly Used Epithelial Cell Line: T84 Intestinal Epithelial Cells

2011 ◽  
pp. 115-137 ◽  
Author(s):  
Rino P. Donato ◽  
Adaweyah El-Merhibi ◽  
Batjargal Gundsambuu ◽  
Kai Yan Mak ◽  
Emma R. Formosa ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Line ◽  
Intestinal Epithelial Cells ◽  
Epithelial Cell Line ◽  
Intestinal Epithelial

The lack of attachment of transformed embryonic lung epithelial cells to collagen I is corrected by fibronectin and FXIII

1986 ◽  
Vol 86 (1) ◽  
pp. 95-107
Author(s):  
M. Paye ◽  
C.M. Lapiere
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Line ◽  
Lung Epithelial Cells ◽  
Collagen I ◽  
Epithelial Cell Line ◽  
Embryonic Lung ◽  
Lung Epithelial ◽  
Minimal Concentration ◽  
Pulmonary Epithelial Cell

PER cells, a transformed pulmonary epithelial cell line that adhered to a large extent to a fibronectin substratum, were found to be attachment-deficient to collagen I. Although fibronectin can bind to collagen I monomers and polymers, the addition of exogenous fibronectin in the attachment medium induced the adhesion of these cells to collagen I polymers but not to monomers. By adding the transglutaminase of blood coagulation, FXIII, in the presence of fibronectin, the attachment of PER cells to collagen I monomers could be recovered while the minimal concentration of fibronectin needed to promote their adhesion to polymers was lowered. These studies indicate that FXIII enhances the fibronectin-mediated attachment of PER cells to collagen I.

Basolateral secretion of kappa light chain in the polarised epithelial cell line, Caco-2

1989 ◽  
Vol 94 (2) ◽  
pp. 327-332
Author(s):  
E.J. Hughson ◽  
D.F. Cutler ◽  
C.R. Hopkins
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Line ◽  
Light Chain ◽  
Intracellular Trafficking ◽  
Epithelial Cell Line ◽  
Kappa Light Chain ◽  
Immunoglobulin Kappa ◽  
Selective Delivery ◽  
Secretory Products

The immunoglobulin kappa light chain is constitutively secreted in non-polarised cells. It is therefore unlikely to display any of the signals thought to be required for the selective delivery of proteins to the apical or basolateral borders of polarised epithelial cells. We have transfected the gene for the kappa light chain into a polarised epithelial cell line (Caco-2) and shown that it is secreted predominantly from the basolateral surface. Metabolically labelled endogenous secretory products show the same polarity and we conclude, therefore, that in Caco-2 cells there is a major intracellular trafficking route to the basolateral border that requires no sorting signal.

scholarly journals Listeria monocytogenes Infection of Bat Pipistrellus nathusii Epithelial cells Depends on the Invasion Factors InlA and InlB

Pathogens ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 867
Author(s):  
Olga Povolyaeva ◽  
Yaroslava Chalenko ◽  
Egor Kalinin ◽  
Olga Kolbasova ◽  
Elena Pivova ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Line ◽  
Domestic Animals ◽  
Epithelial Cell Line ◽  
Intracellular Pathogen ◽  
Wild Type ◽  
Listeria Monocytogenes Infection ◽  
Natural Hosts

L. monocytogenes is a widespread facultative intracellular pathogen. The range of natural hosts that supporting L. monocytogenes persistence in the environment has not been fully established yet. In this study, we were interested in the potential of L. monocytogenes to infect cells of bats, which are being increasingly recognized as a reservoir for microorganisms that are pathogenic to humans and domestic animals. A stable epithelial cell line was developed from the kidneys of Pipistrellus nathusii, a small bat widely distributed across Europe. The wild-type L. monocytogenes strain EGDe infected this cell line with an invasion efficiency of 0.0078 ± 0.0009%. Once it entered bat cells, L. monocytogenes doubled within about 70 min. When L. monocytogenes lacked either of the major invasion factors, InlA and InlB, invasion efficiency decreased by a factor of 10 and 25 respectively (p < 0.000001). The obtained results suggest that bat epithelial cells are susceptible to L. monocytogenes infection and that L. monocytogenes invasion of bat cells depends on the major invasion factors InlA and InlB. These results constitute the first report on in vitro studies of L. monocytogenes infection in bats.

scholarly journals Mechanism of cholera toxin action on a polarized human intestinal epithelial cell line: role of vesicular traffic

1992 ◽  
Vol 117 (6) ◽  
pp. 1197-1209 ◽  
Author(s):  
WI Lencer ◽  
C Delp ◽  
MR Neutra ◽  
JL Madara
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cholera Toxin ◽  
Cell Line ◽  
Intestinal Epithelial Cell ◽  
Time Course ◽  
Epithelial Cell Line ◽  
Intestinal Epithelial ◽  
Vesicular Traffic ◽  
Intestinal Epithelial Cell Line

The massive secretion of salt and water in cholera-induced diarrhea involves binding of cholera toxin (CT) to ganglioside GM1 in the apical membrane of intestinal epithelial cells, translocation of the enzymatically active A1-peptide across the membrane, and subsequent activation of adenylate cyclase located on the cytoplasmic surface of the basolateral membrane. Studies on nonpolarized cells show that CT is internalized by receptor-mediated endocytosis, and that the A1-subunit may remain membrane associated. To test the hypothesis that toxin action in polarized cells may involve intracellular movement of toxin-containing membranes, monolayers of the polarized intestinal epithelial cell line T84 were mounted in modified Ussing chambers and the response to CT was examined. Apical CT at 37 degrees C elicited a short circuit current (Isc: 48 +/- 2.1 microA/cm2; half-maximal effective dose, ED50 integral of 0.5 nM) after a lag of 33 +/- 2 min which bidirectional 22Na+ and 36Cl- flux studies showed to be due to electrogenic Cl- secretion. The time course of the CT-induced Isc response paralleled the time course of cAMP generation. The dose response to basolateral toxin at 37 degrees C was identical to that of apical CT but lag times (24 +/- 2 min) and initial rates were significantly less. At 20 degrees C, the Isc response to apical CT was more strongly inhibited (30-50%) than the response to basolateral CT, even though translocation occurred in both cases as evidenced by the formation of A1-peptide. A functional rhodamine-labeled CT-analogue applied apically or basolaterally at 20 degrees C was visualized only within endocytic vesicles close to apical or basolateral membranes, whereas movement into deeper apical structures was detected at 37 degrees C. At 15 degrees C, in contrast, reduction to the A1-peptide was completely inhibited and both apical and basolateral CT failed to stimulate Isc although Isc responses to 1 nM vasoactive intestinal peptide, 10 microM forskolin, and 3 mM 8Br-cAMP were intact. Re-warming above 32 degrees C restored CT-induced Isc. Preincubating monolayers for 30 min at 37 degrees C before cooling to 15 degrees C overcame the temperature block of basolateral CT but the response to apical toxin remained completely inhibited. These results identify a temperature-sensitive step essential to apical toxin action on polarized epithelial cells. We suggest that this event involves vesicular transport of toxin-containing membranes beyond the apical endosomal compartment.

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