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PubMed1992

Epstein-Barr virus enters B cells and epithelial cells by different routes.

Epstein-Barr virus (EBV) infects two cell types, B lymphocytes and epithelial cells. Electron microscopic studies have shown that the virus fuses with the lymphoblastoid cell line Raji but is endocytosed into thin-walled non-clathrin-coated vesicles in normal B cells before fusion takes place. To compare early interactions of EBV with epithelial cells and B cells, a fluorescence dequenching assay of fusion was employed, using virus labeled either with the pH-insensitive probe octadecyl rhodamine B chloride (R18) or with 5(N-octadecanoyl) aminofluorescein (AF), which loses emission intensity at a pH below 7.4. Fusion of virus labeled with R18 could be monitored with B cells, Raji cells, and epithelial cells. Lowering the extracellular pH or pretreatment of cells with ammonium chloride or methylamine had no effect on these measurements. In contrast, fusion of virus labeled with AF could be measured with Raji cells and epithelial cells, but not with normal B cells unless cells were previously treated with ammonium chloride. Fusion of virus with normal B cells was inhibited with chlorpromazine, chloroquine, and sodium azide, but none of these reagents had any effect on fusion with Raji or epithelial cells. These results suggest that entry of EBV into nonpolarized suspensions of epithelial cells occurs by fusion at the cell surface, that EBV may be incapable of fusing with normal B cells unless it has first been endocytosed, and that pH appears to be irrelevant to either event. A combination of the two probes, R18 and AF, may have general use for determining the sites of entry of enveloped viruses that fuse in a pH-independent manner.

Attachment Sites, Microbiological↗

PubMed1992

Growth of epithelial cells in the thymic medulla is under the control of mature T cells.

Epithelial cells in the thymic medulla are conspicuous in normal adult mice, but sparse in the early fetal thymus and the thymus of adult T cell-deficient SCID mice. To examine whether growth of medullary epithelial cells (MEC) depends upon local contact with mature T cells, we used the finding that the SCID thymus is unusually permeable to mature T cells entering from the bloodstream. When SCID mice received multiple injections of mature lymph node T cells from birth, the thymus accumulated large numbers of mature TCR+ T cells of resting phenotype, but contained virtually no immature (CD4+8+) cells. The injected T cells localized in the medullary region of the thymus and led to marked regeneration of MEC. These and other data suggest that the growth of MEC is under the control of mature T cells. Placing MEC under T cell control might be a device for regulating the size and integrity of the medulla, especially during the phase of rapid thymic growth. Maintaining the cellular components of the medulla in proper balance could be critical for ensuring efficient self tolerance induction.

Animals↗

PubMed1990

Human oral epithelial cell culture. II. Keratin expression in fetal and adult gingival cells.

Epithelial cells from human fetal and adult gingiva were cultured in keratinocyte growth medium (KGM), a serum-free medium. The expression of keratin proteins in these cells was evaluated using immunohistochemistry and SDS-PAGE-immunoblot analysis and compared with expression in the tissue. Keratins 5, 6, 14, 16, and 19 were identified in cells cultured from both fetal and adult tissues. K19 was localized in basal cells of fetal oral tissue but was not seen in adult gingiva (except for scattered Merkel cells). K1 and K10 were expressed in tissue, but not in cultured cells. The keratin profiles of cultured epithelial cells from several adult donors were similar and were identical in cultures from primary through Passage 5. K13, a differentiation-specific keratin, was expressed in all suprabasal cells of fetal oral epithelium, but shows only spotty expression in adult gingival tissue. K13 was expressed in cultures of fetal cells, but very weakly or not at all in cultures of adult cells. K13 expression was greater in cultures grown with physiologic calcium concentrations (1.2 mM) than in those grown at 0.15 mM or less. Our findings are consistent with basal-like characters of these cells in 0.15 mM calcium growth conditions. Differentiation of fetal oral cells in culture to the suprabasal basal cell stage in 1.2 mM Ca2+ is shown by the expression of K13.

Adult↗

PubMed2000

Epstein-Barr virus lacking glycoprotein gp85 cannot infect B cells and epithelial cells.

To evaluate whether the BXLF2 gene of Epstein-Barr virus (EBV), which codes gp85 protein, is essential for infection of B cells and epithelial cells, we analyzed the infectivity of an EBV recombinant lacking gp85. The cells that were infected with the BXLF2-disrupted virus were unable to express gp85 proteins that could be detected by mouse monoclonal antibody E1D1, specific for gp85/gp25 complexes. The BXLF2-disrupted EBV had the ability to attach to, but not infect, B cells. On the other hand, the same virus failed to bind to and infect NU-GC-3, a human gastric adenocarcinoma cell line that is susceptible to EBV infection. The results indicate that the gp85 is used for infection of not only B cells but also epithelial cells and suggest that the gp85 is necessary for attaching the virus to epithelial cells.

Animals↗

PubMed2004

Transcriptome analysis and gene expression profiles of early apoptosis-related genes in Streptococcus pyogenes-infected epithelial cells.

Epithelial cells are the initial sites of host invasion by group A Streptococcus pyogenes (GAS), and GAS infection of epithelial cells has been suggested to induce apoptosis. We previously reported that the induction of apoptosis is strongly associated with the protein F1-mediated invasion. We present here the gene expression profiles of the human epithelial HEp-2 cells during GAS-induced apoptosis, using serial gene analysis of expression (SAGE) analysis and macroarray analysis of apoptosis-related genes. Serial gene analysis of expression revealed the downregulation of voltage-dependent anion channels 1 and 2 genes and the upregulation of the cytochrome c oxidase and calcium binding protein genes (calpactin, calgizzarin and programmed cell death 6). Macroarray analysis and quantitative RT-PCR analysis also revealed that the genes for IL-1beta, IL-12 p35, IL12 p40, and GM-CSF are also markedly induced by GAS invasion. Furthermore, caspase-1, -9, and -14 genes are significantly upregulated during GAS invasion. These observations indicated that apoptosis associated with GAS invasion is mainly induced by mitochondrial dysfunction and calcium regulation as well as by stress, and that these transcriptional controls may regulate the cellular response to GAS invasion.

Apoptosis↗

PubMed2001

Endometrial stromal cells regulate epithelial cell growth in vitro: a new co-culture model.

The regulation of epithelial cell function and morphogenesis by the paracrine effectors from the mesenchyme or stroma has been well established using in-vivo studies. A more complete understanding of these relationships has been delayed due, in part, to a lack of appropriate co-culture models. In this study, we describe a co-culture model which demonstrates that normal paracrine relationships can be reconstituted in vitro and that human endometrial stromal cells regulate both growth and differentiation of primary human endometrial epithelial cells. Interesting differences in the proliferation of stromal and epithelial cells were noted in response to the basement membrane extract, Matrigel((R)). Exposure of stromal cells to Matrigel((R)) enhanced the paracrine capacity of these cells in vitro. When epithelial cells were co-cultured in contact with stromal cells embedded in Matrigel((R)), epithelial cell growth was inhibited by 65-80% compared to controls. Stromal cells in contact with Matrigel((R)) also regulated epithelial cell differentiation, as shown by induction of glycodelin expression. These co-culture studies show great promise as a method to investigate the cellular interactions between endometrial stromal and epithelial cells and their environment and to understand the molecular basis for the regulation of normal growth and differentiation of cells within complex tissues such as the endometrium.

Adult↗

PubMed1992

Biological characteristics of primary cultures of human gallbladder epithelial cells.

Epithelial cells of the gallbladder have potential to represent an important model for studies of ductal epithelial in normal and pathological states. We therefore initiated studies to establish human gallbladder epithelial cells (GBEC) in culture. GBEC were isolated by trypsinization of small tissue fragments from human gallbladders obtained at cholecystectomy; cells were plated on tissue culture dishes and grown in defined MCDB 153 medium containing added growth factors. In this medium, GBEC showed a plating efficiency of approximately 1%; those GBEC that attached formed colonies and proliferated, as demonstrated by autoradiographic analysis of [3H]thymidine incorporation into DNA. Cultured GBEC expressed two markers found on GBEC in situ, i.e., gamma-glutamyl transpeptidase and cytokeratin 19. By using various attachment substrates, with and without added serum, increased plating efficiency and better growth were achieved. When type IV collagen was used as substrate and 10% fetal bovine serum was added to MCDB 153, passage of GBEC was possible, and cells proliferated through five to six population doublings. GBEC in culture under all conditions eventually enlarged, showed vacuolization, and demonstrated irreversible growth arrest. Nonetheless, the culture conditions described here allow for preparation of large quantities of highly enriched human GBEC.

Cell Division↗

PubMed2001

The expression of Bok is regulated by serum in HC11 mammary epithelial cells.

Epithelial cells within the mammary gland undergo apoptosis during weaning. To determine the expression of Bok mRNA (a member of the pro-apoptotic Bcl-2 family) in the mammary gland and its regulation, we examined the expression of the Bok transcript in the mouse mammary gland and HC11 mammary epithelial cells in culture through RT-PCR. The Bok mRNA expression was found in the mammary gland. The expression of the Bok mRNA level was induced through serum starvation and overexpression of Bok induced apoptosis in HC11 cells in culture. These results indicate that the expression of Bok mRNA in the mammary gland is regulated through serum starvation. It also may be related to the mammary involution.

Animals↗

PubMed2005

Ontogeny and regulation of IL-7-expressing thymic epithelial cells.

Epithelial cells in the thymus produce IL-7, an essential cytokine that promotes the survival, differentiation, and proliferation of thymocytes. We identified IL-7-expressing thymic epithelial cells (TECs) throughout ontogeny and in the adult mouse thymus by in situ hybridization analysis. IL-7 expression is initiated in the thymic fated domain of the early primordium by embryonic day 11.5 and is expressed in a Foxn1-independent pathway. Marked changes occur in the localization and regulation of IL-7-expressing TECs during development. IL-7-expressing TECs are present throughout the early thymic rudiment. In contrast, a major population of IL-7-expressing TECs is localized to the medulla in the adult thymus. Using mouse strains in which thymocyte development is arrested at various stages, we show that fetal and postnatal thymi differ in the frequency and localization of IL-7-expressing TECs. Whereas IL-7 expression is initiated independently of hemopoietic-derived signals during thymic organogenesis, thymocyte-derived signals play an essential role in regulating IL-7 expression in the adult TEC compartment. Moreover, different thymocyte subsets regulate the expression of IL-7 and keratin 5 in adult cortical epithelium, suggesting that despite phenotypic similarities, the cortical TEC compartments of wild-type and RAG-1(-/-) mice are developmentally and functionally distinct.

Animals↗

PubMed1996

A murine and a porcine coronavirus are released from opposite surfaces of the same epithelial cells.

Epithelial cells are important target cells for coronavirus infection. Earlier we have shown that transmissible gastroenteritis coronavirus (TGEV) and mouse hepatitis coronavirus (MHV) are released from different sides of porcine and murine epithelial cells, respectively. To study the release of these viruses from the same cells, we constructed a porcine LLC-PK1 cell line stably expressing the recombinant MHV receptor cDNA (LMR cells). The MHV and TGEV receptor glycoproteins were shown by immunofluorescence to appear at the surface of the cells and to be functional so that the cells were susceptible to both MHV and TGEV infection. Both coronaviruses entered polarized LMR cells only through the apical surface. Remarkably, while the cells remained susceptible to TGEV for long periods, infectability by MHV decreased with time after plating of the cells onto filters. This was not due to a lack of expression of the MHV receptor, since this glycoprotein was still abundant on the apical surface of these cells. TGEV and MHV appeared to exit LMR cells from opposite sides. Whereas TGEV was released preferentially at the apical membrane, MHV was released preferentially at the basolateral surface. These results show that vesicles containing the two coronaviruses are targeted differently in LMR cells. We propose that the viruses are sorted at the Golgi complex into different transport vesicles that carry information directing them to one of the two surface domains. The apical release of TGEV and the basolateral release of MHV might be factors contributing to the difference in virus spread found between TGEV and MHV in their respective natural hosts, the former causing mainly a localized enteric infection, the latter spreading through the body to other organs.

Animals↗

PubMed1993

CD1d is involved in T cell-intestinal epithelial cell interactions.

We assessed the role of the nonclassical class I molecule, CD1d, in the interaction between intestinal epithelial cells and T cells. In a mixed lymphocyte reaction (MLR) system where the stimulator cells were irradiated normal intestinal cells, the anti-CD1d monoclonal antibody (mAb) 3C11 inhibited T cell proliferation. In contrast, no inhibition was seen when mAb 3C11 was added to conventional MLR cultures (non T cell stimulators). Furthermore, no inhibition was seen when either airway epithelial cells were used as stimulator cells or lamina propria lymphocytes were used as responder cells. These latter two conditions along with a conventional MLR favor CD4+ T cell proliferation. However, we have previously shown that normal intestinal epithelial cells stimulate CD8+ T cells under similar culture conditions. Thus, CD1d expressed on intestinal epithelial cells may be an important ligand in CD8+ T cell-epithelial cell interactions.

Antibodies, Monoclonal↗

PubMedDate not supplied

Ion transport processes of crustacean epithelial cells.

Epithelial cells of the gut, antennal glands, integument, and gills of crustaceans regulate the movements of ions into and across these structures and thereby influence the concentrations of ions in the hemolymph. Specific transport proteins serving cations and anions are found on apical and basolateral cell membranes of epithelia in these tissues. In recent years, a considerable research effort has been directed at elucidating their physiological and molecular properties and relating these characteristics to the overall biology of the organisms. Efforts to describe ion transport in crustaceans have focused on the membrane transfer properties of Na+/H+ exchange, calcium uptake as it relates to the molt cycle, heavy metal sequestration and detoxification, and anion movements into and across epithelial cells. In addition to defining the properties and mechanisms of cation movements across specific cell borders, work over the past 5 yr has also centered on defining the molecular nature of certain transport proteins such as the Na+/H+ exchanger in gill and gut tissues. Monovalent anion transport proteins of the gills and gut have received attention as they relate to osmotic and ionic balance in euryhaline species. Divalent anion secretion events of the gut have been defined relative to potential roles they may have in hyporegulation of the blood and in hepatopancreatic detoxification events involving complexation with cationic metals.

Amino Acid Sequence↗

PubMed1990

Comparison of the function of the tight junctions of endothelial cells and epithelial cells in regulating the movement of electrolytes and macromolecules across the cell monolayer.

In cell culture, both endothelial and epithelial cell monolayers have been found to generate structurally similar tight junctional complexes, as assessed by thin complexes of the two cell types are, at least in part, responsible for the very different permeability characteristics of native endothelial and epithelial cell monolayers. The purpose of this work was to compare cultured endothelial and epithelial cells with respect to the function of their tight junctional complexes in regulating the movement of macromolecules and ions across the cell monolayers, and define functional parameters to characterize the tight junctional complexes. Bovine aorta endothelial cells and T84 colonic carcinoma epithelial cells were cultured on a microporous membrane support. The permeability coefficients of inulin, albumin, and insulin were determined with the cell monolayers and compared with the permeability coefficients obtained with 3T3-C2 fibroblasts, a cell line that does not generate tight junctions. Electrical resistance measurements across the monolayer-filter systems were also compared. The permeability coefficient of albumin across the endothelial cell monolayer compared favorably with other reported values. Likewise, the electrical resistance across the T84 cell monolayer was in good agreement with published values. Utilizing permeability coefficients for macromolecules as an index of tight junction function, we found that a distinction between a lack of tight junctions (fibroblasts), the presence of endothelial tight junctions, and the presence of epithelial tight junctions was readily made. However, when utilizing electrical resistance as an index of tight junction function, identical measurements were obtained with fibroblasts and endothelial cells. This indicates that more than one index of tight junction function is necessary to characterize the junctional complexes. Although structurally similar, epithelial cell and endothelial cell tight junctions perform very different functions, and, from our data, we conclude that the demonstration of tight junctional structures by electron microscopy is not relevant to the functional nature of the junction: structure does not imply function. A minimal assessment of tight junction function should rely on both the determination of the electrical resistance across the cell monolayer, and the determination of the permeability coefficients of selected macromolecules.

Animals↗

PubMed2003

The other cells in asthma: dendritic cell and epithelial cell crosstalk.

Dendritic cells (DCs) and epithelial cells are the first cells to encounter inhaled allergens. The response of these cell types to allergens is fundamentally different in asthmatics compared with nonasthmatics. DCs and epithelial cells interact through cell-cell interactions and through release of soluble mediators. The response of epithelial cells to allergens can profoundly modify the behavior of intramucosal DCs. Upon migration to the draining nodes, mucosal DCs undergo functional maturation and induce proliferation in naive T cells and primed Th2 cells. The implications of the DC-epithelial interaction for the pathogenesis of asthma is becoming increasingly clear by the use of mouse models and culture systems of human cells.

Animals↗

PubMed1977

Contribution of mucosal chloride to chloride in toad bladder epithelial cells.

Epithelial cells were scraped from the bladders of toads of the species Bufo marinus obtained from the Dominican Republic. These epithelial cells exchanged their chloride virtually completely with 36Cl i; the medium within 60 min. Of this chloride, about 93% came from the serosal medium. The approximately 20 mmole/kg dry wt of chloride which equilibrates with 36Cl in the mucosal medium was still present when choline replaced sodium in the medium in the presence of amiloride (10(-4) M) and was almost all readily removed by rapid washing of the mucosal surface immediately prior to analysis. These observations suggest that little chloride of mucosal origin is truly intracellular. This conclusion is supported by the fact that after vasopressin the increased cellular chloride was not of mucosal origin.

Animals↗

PubMed1995

Polarized entry of bovine coronavirus in epithelial cells.

Epithelial cells are highly polarized cells divided into an apical and a basolateral plasma membrane. The two domains are composed of a distinct set of proteins and lipids. Concerning virus infection of epithelial cells, the polarity of host cell receptor distribution defines the domain from which infection may be mediated. We were interested to analyze the infection of polarized cells by bovine coronavirus (BCV). The entry of BCV into MDCK I cells was investigated by growing the cells on a permeable support. Cell were infected with BCV from either the apical or basolateral domain. The efficiency of infection was determined by measuring the hemaglutinating activity of the virus released into the apical compartment. Virus replication was only detectable after inoculation from the apical surface. Therefore, infection of MDCK I cells with BCV is restricted to the apical side.

Animals↗

PubMed1989

Decay accelerating factor regulates complement activation on glomerular epithelial cells.

Epithelial cells of the glomerular capillary are the site of C5b-9 mediated injury in rat membranous nephropathy. We investigated the regulation of C activation by cultured glomerular epithelial cells (GEC). Rat and human GEC were more resistant to C injury by homologous C than heterologous C. In human GEC homologous C cytotoxicity was enhanced by antiserum to decay accelerating factor (DAF) indicating that homologous C activation was, at least in part, restricted by membrane DAF. Anti-DAF immunoprecipitated a 67-kDa protein from human glomeruli. In rat GEC, pronase and phosphatidylinositol-specific phospholipase C (which are known to inactivate human DAF) enhanced cytotoxicity by homologous C. Thus, DAF is present on human GEC in culture and in human kidney glomeruli, and a DAF-like protein is present on cultured rat GEC. These proteins regulate C activation in vitro and may play a role in controlling C activation on GEC in vivo.

Animals↗

PubMed1997

Nitric oxide activates chloride currents in human lung epithelial cells.

Epithelial Cl- channels are regulated by various physiological factors, including guanosine 3',5'-cyclic monophosphate (cGMP). Because cGMP mediates many of the physiological actions of nitric oxide (NO), we have studied both the presence of endogenous NO and the effects of exogenous NO on Cl- currents in A549 human lung epithelial cells. We have detected Ca(2+)-dependent NO synthase activity in A549 cells. Using the perforated patch-clamp technique, we have shown that inhibition of this enzyme by NG-monomethyl-L-arginine decreased Cl- current, an effect that was reversed by the NO donor S-nitrosoglutathione (GSNO). In addition, the NO donors GSNO and S-nitroso-N-acetyl-D,L-penicillamine increased whole-cell Cl- currents in A549 cells. This stimulatory effect of the NO donors was sensitive to inhibition by 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid, suggesting that channels other than the cystic fibrosis transmembrane conductance regulator (CFTR) are involved in the action of NO on A549 cells. In addition, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, a selective inhibitor of soluble guanylyl cyclase, decreased NO-mediated stimulation of Cl- currents. Our results suggest that, in lung epithelial cells, NO regulates a non-CFTR Cl- conductance acting via a cGMP-dependent mechanism.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗