Effects of eight antibacterial agents on cell survival and expression of epithelial-cell- or cell-adhesion-related genes in human gingival epithelial cells

Inside the thymus, thymic epithelial cells and thymocytes show an interdependent relationship for their functional differentiation and development. As regards possible interdependency for their mutual survival, it is clear that lympho-epithelial adhesion can control the survival of developing thymocytes whereas the effects of lymphoid adhesion on epithelial cell survival have never been described. To address this issue, we performed co-cultures between normal human thymic epithelial cells (TEC) and a mature lymphoid T cell line (H9) or unfractionated thymocytes. TEC were induced to apoptosis by growth factor deprivation and the level of cell death was measured by flow cytometry. TEC stimulated by cell adhesion showed a significant reduced apoptosis when compared to the control and this phenomenon was associated with increased binding activity of NF-(kappa)B, as measured by gel shift analysis. The activation of NF-(kappa)B was necessary to promote survival, since its inhibition by acetyl salicylic acid prevented the promoting effect. The mAb-mediated crosslinking of (alpha)(3)(beta)(1) was considered as a potential inducer of TEC survival, since we have previously demonstrated that the engagement of this integrin was able to induce NF-(kappa)B activation in TEC. The crosslinking of (alpha)(3)(beta)(1), which clustered at the lympho-epithelial contact sites, partially reproduced the promoting activity of cell adhesion. These results highlight that lympho-epithelial adhesion can control the survival of thymic epithelial cells through an intracellular pathway which requires the activation of NF-(kappa)B and is triggered by integrins of the (beta)(1) family.

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Influence of Porphyromonas gingivalis on the Expression of Cell Adhesion Molecules and Apoptosis in Human Gingival Epithelial Cells

Journal of Oral Biosciences ◽

10.1016/s1349-0079(06)80023-x ◽

2006 ◽

Vol 48 (2) ◽

pp. 103-113

Author(s):

Shintaro Hata ◽

Akio Tanaka

Keyword(s):

Cell Adhesion ◽

Epithelial Cells ◽

Adhesion Molecules ◽

Porphyromonas Gingivalis ◽

Cell Adhesion Molecules ◽

Gingival Epithelial Cells ◽

Human Gingival Epithelial Cells

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Aggregatibacter actinomycetemcomitans regulates the expression of integrins and reduces cell adhesion via integrin α5 in human gingival epithelial cells

Molecular and Cellular Biochemistry ◽

10.1007/s11010-017-3076-z ◽

2017 ◽

Vol 436 (1-2) ◽

pp. 39-48 ◽

Cited By ~ 1

Author(s):

Shinsuke Kochi ◽

Keisuke Yamashiro ◽

Shoichi Hongo ◽

Tadashi Yamamoto ◽

Yuki Ugawa ◽

...

Keyword(s):

Cell Adhesion ◽

Epithelial Cells ◽

Aggregatibacter Actinomycetemcomitans ◽

Gingival Epithelial Cells ◽

Integrin Α5 ◽

Human Gingival Epithelial Cells

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Cigarette Smoke Stimulates SARS-CoV-2 Internalization by Activating AhR and Increasing ACE2 Expression in Human Gingival Epithelial Cells

International Journal of Molecular Sciences ◽

10.3390/ijms22147669 ◽

2021 ◽

Vol 22 (14) ◽

pp. 7669

Author(s):

Cassio Luiz Coutinho Almeida-da-Silva ◽

Harmony Matshik Dakafay ◽

Kaitlyn Liu ◽

David M. Ojcius

Keyword(s):

Epithelial Cells ◽

Oral Cavity ◽

Cigarette Smoke ◽

Large Body ◽

Receptor Expression ◽

Host Cells ◽

Dependent Manner ◽

Gingival Epithelial Cells ◽

Human Gingival Epithelial Cells ◽

Oral Cells

A large body of evidence shows the harmful effects of cigarette smoke to oral and systemic health. More recently, a link between smoking and susceptibility to coronavirus disease 2019 (COVID-19) was proposed. COVID-19 is due to infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which uses the receptor ACE2 and the protease TMPRSS2 for entry into host cells, thereby infecting cells of the respiratory tract and the oral cavity. Here, we examined the effects of cigarette smoke on the expression of SARS-CoV-2 receptors and infection in human gingival epithelial cells (GECs). We found that cigarette smoke condensates (CSC) upregulated ACE2 and TMPRSS2 expression in GECs, and that CSC activated aryl hydrocarbon receptor (AhR) signaling in the oral cells. ACE2 was known to mediate SARS-CoV-2 internalization, and we demonstrate that CSC treatment potentiated the internalization of SARS-CoV-2 pseudovirus in GECs in an AhR-dependent manner. AhR depletion using small interference RNA decreased SARS-CoV-2 pseudovirus internalization in CSC-treated GECs compared with control GECs. Our study reveals that cigarette smoke upregulates SARS-CoV-2 receptor expression and infection in oral cells. Understanding the mechanisms involved in SARS-CoV-2 infection in cells of the oral cavity may suggest therapeutic interventions for preventing viral infection and transmission.

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Redistribution and dysfunction of integrins in cultured renal epithelial cells exposed to oxidative stress

AJP Renal Physiology ◽

10.1152/ajprenal.1993.264.1.f149 ◽

1993 ◽

Vol 264 (1) ◽

pp. F149-F157 ◽

Cited By ~ 14

Author(s):

J. Gailit ◽

D. Colflesh ◽

I. Rabiner ◽

J. Simone ◽

M. S. Goligorsky

Keyword(s):

Oxidative Stress ◽

Cell Adhesion ◽

Epithelial Cell ◽

Epithelial Cells ◽

Cell Surface ◽

Apical Cell ◽

Flow Cytometric Analysis ◽

Adhesion Properties ◽

Renal Tubular Cells ◽

Renal Tubular

Tubular obstruction by detached renal tubular epithelial cells is a major cause of oliguria in acute renal failure. Viable renal tubular cells can be recovered from urine of patients with acute tubular necrosis, suggesting a possible defect in cell adhesion to the basement membrane. To study this process of epithelial cell desquamation in vitro, we investigated the effect of nonlethal oxidative stress on the integrin adhesion receptors of the primate kidney epithelial cell line BS-C-1. Morphological and functional studies of cell adhesion properties included the following: interference reflection microscopy, intravital confocal microscopy and immunocytochemistry, flow cytometric analysis of integrin receptor abundance, and cell-matrix attachment assay. High levels of the integrin subunits alpha 3, alpha v, and beta 1 were detected on the cell surface by fluorescence-activated cell sorting (FACS) analysis, as well as lower levels of alpha 1, alpha 2, alpha 4, alpha 5, alpha 6, and beta 3. Exposure of BS-C-1 cells to nonlethal oxidative stress resulted in the disruption of focal contacts, disappearance of talin from the basal cell surface, and in the redistribution of integrin alpha 3-subunits from predominantly basal location to the apical cell surface. As measured in a quantitative cell attachment assay, oxidative stress decreased BS-C-1 cell adhesion to type IV collagen, laminin, fibronectin, and vitronectin. Defective adhesion was not associated with a loss of alpha 3-, alpha 4-, or alpha v-integrin subunits from the cell surface.(ABSTRACT TRUNCATED AT 250 WORDS)

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Pro-inflammatory cytokine responses in human gingival epithelial cells after stimulation with cell wall extract of Aggregatibacter actinomycetemcomitans subtypes

Anaerobe ◽

10.1016/j.anaerobe.2017.08.001 ◽

2017 ◽

Vol 48 ◽

pp. 103-109 ◽

Cited By ~ 5

Author(s):

Nuntiya Pahumunto ◽

Pareena Chotjumlong ◽

Anupong Makeudom ◽

Suttichai Krisanaprakornkit ◽

Gunnar Dahlen ◽

...

Keyword(s):

Cell Wall ◽

Epithelial Cells ◽

Inflammatory Cytokine ◽

Aggregatibacter Actinomycetemcomitans ◽

Cytokine Responses ◽

Gingival Epithelial Cells ◽

Cell Wall Extract ◽

Human Gingival Epithelial Cells

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Regulation of epithelial and lymphocyte cell adhesion by adenosine deaminase–CD26 interaction

Biochemical Journal ◽

10.1042/bj3610203 ◽

2002 ◽

Vol 361 (2) ◽

pp. 203-209 ◽

Cited By ~ 4

Author(s):

Silvia GINÉS ◽

Marta MARIÑO ◽

Josefa MALLOL ◽

Enric I. CANELA ◽

Chikao MORIMOTO ◽

...

Keyword(s):

T Cells ◽

Cell Adhesion ◽

T Cell ◽

B Cells ◽

Epithelial Cell ◽

Epithelial Cells ◽

Cell Surface ◽

Adenosine Deaminase ◽

Cell To Cell Adhesion ◽

Lymphocyte Cell

The extra-enzymic function of cell-surface adenosine deaminase (ADA), an enzyme mainly localized in the cytosol but also found on the cell surface of monocytes, B cells and T cells, has lately been the subject of numerous studies. Cell-surface ADA is able to transduce co-stimulatory signals in T cells via its interaction with CD26, an integral membrane protein that acts as ADA-binding protein. The aim of the present study was to explore whether ADA—CD26 interaction plays a role in the adhesion of lymphocyte cells to human epithelial cells. To meet this aim, different lymphocyte cell lines (Jurkat and CEM T) expressing endogenous, or overexpressing human, CD26 protein were tested in adhesion assays to monolayers of colon adenocarcinoma human epithelial cells, Caco-2, which express high levels of cell-surface ADA. Interestingly, the adhesion of Jurkat and CEM T cells to a monolayer of Caco-2 cells was greatly dependent on CD26. An increase by 50% in the cell-to-cell adhesion was found in cells containing higher levels of CD26. Incubation with an anti-CD26 antibody raised against the ADA-binding site or with exogenous ADA resulted in a significant reduction (50–70%) of T-cell adhesion to monolayers of epithelial cells. The role of ADA—CD26 interaction in the lymphocyte—epithelial cell adhesion appears to be mediated by CD26 molecules that are not interacting with endogenous ADA (ADA-free CD26), since SKW6.4 (B cells) that express more cell-surface ADA showed lower adhesion than T cells. Adhesion stimulated by CD26 and ADA is mediated by T cell lymphocyte function-associated antigen. A role for ADA—CD26 interaction in cell-to-cell adhesion was confirmed further in integrin activation assays. FACS analysis revealed a higher expression of activated integrins on T cell lines in the presence of increasing amounts of exogenous ADA. Taken together, these results suggest that the ADA—CD26 interaction on the cell surface has a role in lymphocyte—epithelial cell adhesion.

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Identification of Porphyromonas gingivalis Genes Specifically Expressed in Human Gingival Epithelial Cells by Using Differential Display Reverse Transcription-PCR

Infection and Immunity ◽

10.1128/iai.72.7.3752-3758.2004 ◽

2004 ◽

Vol 72 (7) ◽

pp. 3752-3758 ◽

Cited By ~ 34

Author(s):

Yoonsuk Park ◽

Özlem Yilmaz ◽

Il-Young Jung ◽

Richard J. Lamont

Keyword(s):

Epithelial Cells ◽

Porphyromonas Gingivalis ◽

Abc Transporter ◽

Differential Display ◽

Molecular Mechanisms ◽

Gene Products ◽

Reverse Transcription Pcr ◽

Gingival Epithelial Cells ◽

Insertional Inactivation ◽

Human Gingival Epithelial Cells

ABSTRACT Porphyromonas gingivalis, one of the causative agents of adult periodontitis, can invade and survive within host epithelial cells. The molecular mechanisms by which P. gingivalis induces uptake and adapts to an intracellular environment are not fully understood. In this study, we have investigated the genetic responses of P. gingivalis internalized within human gingival epithelial cells (GECs) in order to identify factors involved in invasion and survival. We compared the differential display of arbitrarily PCR-amplified gene transcripts in P. gingivalis recovered from GECs with the display of transcripts in P. gingivalis control cultures. Over 20 potential differentially expressed transcripts were identified. Among these, pepO, encoding an endopeptidase, and genes encoding an ATP-binding cassette (ABC) transporter and a cation-transporting ATPase were upregulated in GECs. To investigate the functionality of these gene products, mutants were generated by insertional inactivation. Compared to the parental strain, mutants of each gene showed a significant reduction in their invasion capabilities. In addition, GEC cytoskeletal responses to the mutants were distinct from those induced by the parent. In contrast, adhesion of the mutant strains to GECs was not affected by lack of expression of the gene products. These results suggest that PepO, a cation-transporting ATPase, and an ABC transporter are required for the intracellular lifestyle of P. gingivalis.

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