In Vitro Studies on Erythrosine-Based Photodynamic Therapy of Malignant and Pre-Malignant Oral Epithelial Cells

Short-chain fatty acids (SCFA), bacterial metabolites released from dental biofilm, are supposed to target the oral epithelium. There is, however, no consensus on how SCFA affect the oral epithelial cells. The objective of the present study was to systematically review the available in vitro evidence of the impact of SCFA on human oral epithelial cells in the context of periodontal disease. A comprehensive electronic search using five databases along with a grey literature search was performed. In vitro studies that evaluated the effects of SCFA on human oral epithelial cells were eligible for inclusion. Risk of bias was assessed by the University of Bristol’s tool for assessing risk of bias in cell culture studies. Certainty in cumulative evidence was evaluated using GRADE criteria (grading of recommendations assessment, development, and evaluation). Of 3591 records identified, 10 were eligible for inclusion. A meta-analysis was not possible due to the heterogeneity between the studies. The risk of bias across the studies was considered “serious” due to the presence of methodological biases. Despite these limitations, this review showed that SCFA negatively affect the viability of oral epithelial cells by activating a series of cellular events that includes apoptosis, autophagy, and pyroptosis. SCFA impair the integrity and presumably the transmigration of leucocytes through the epithelial layer by changing junctional and adhesion protein expression, respectively. SCFA also affect the expression of chemokines and cytokines in oral epithelial cells. Future research needs to identify the underlying signaling cascades and to translate the in vitro findings into preclinical models.

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The effect of secretory immunoglobulin A on the in-vitro adherence of the yeast Candida albicans to human oral epithelial cells

Archives of Oral Biology ◽

10.1016/0003-9969(82)90184-4 ◽

1982 ◽

Vol 27 (8) ◽

pp. 617-621 ◽

Cited By ~ 57

Author(s):

K. Vudhichamnong ◽

D.M. Walker ◽

H.C. Ryley

Keyword(s):

Candida Albicans ◽

Epithelial Cells ◽

Immunoglobulin A ◽

Secretory Immunoglobulin A ◽

Oral Epithelial Cells ◽

Oral Epithelial ◽

Secretory Immunoglobulin

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The Influence of Oral Bacteria on Epithelial Cell MigrationIn Vitro

Mediators of Inflammation ◽

10.1155/2013/154532 ◽

2013 ◽

Vol 2013 ◽

pp. 1-6 ◽

Cited By ~ 17

Author(s):

Alexa M. G. A. Laheij ◽

Johannes J. de Soet ◽

Enno C. I. Veerman ◽

Jan G. M. Bolscher ◽

Cor van Loveren

Keyword(s):

Epithelial Cell ◽

Epithelial Cells ◽

Oral Bacteria ◽

Bacterial Cells ◽

Oral Epithelial Cells ◽

Prevotella Nigrescens ◽

Hematopoetic Stem Cell ◽

Oral Epithelial ◽

Hematopoetic Stem Cell Transplantation

Oral ulcerations often arise as a side effect from chemo- and radiation therapy. In a previous clinical study,Porphyromonas gingivaliswas identified as a positive predictor for oral ulcerations after hematopoetic stem cell transplantation, possibly incriminatingP. gingivalisin delayed healing of the ulcerations. Therefore, it was tested whetherP. gingivalisand its secreted products could inhibit the migration of oral epithelial cells in anin vitroscratch assay. To compare, the oral bacteriaPrevotella nigrescens,Prevotella intermedia,Tannerella forsythia, andStreptococcus mitiswere included. A standardized scratch was made in a confluent layer of human oral epithelial cells. The epithelial cells were challenged with bacterial cells and with medium containing secretions of these bacteria. Closure of the scratch was measured after 17 h using a phase contrast microscope.P. gingivalis,P. nigrescens, and secretions ofP. gingivalisstrongly inhibited cell migration. A challenge with 1000 heat-killed bacteria versus 1 epithelial cell resulted in a relative closure of the scratch of 25% forP. gingivalisand 20% forP. nigrescens. Weaker inhibitory effects were found for the other bacteria. The results confirmed our hypothesis that the oral bacteria may be involved in delayed wound healing.

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Tannerella forsythia invasion in oral epithelial cells requires phosphoinositide 3-kinase activation and clathrin-mediated endocytosis

Microbiology ◽

10.1099/mic.0.048975-0 ◽

2011 ◽

Vol 157 (8) ◽

pp. 2382-2391 ◽

Cited By ~ 14

Author(s):

Elina Mishima ◽

Ashu Sharma

Keyword(s):

Epithelial Cells ◽

Rho Gtpases ◽

Membrane Microdomains ◽

Small Interfering Rnas ◽

Tannerella Forsythia ◽

Lipid Kinase ◽

Signalling Molecules ◽

Oral Epithelial Cells ◽

Oral Epithelial

Tannerella forsythia, a Gram-negative anaerobe implicated in periodontitis, has been detected within human buccal epithelial cells and shown to invade oral epithelial cells in vitro. We have previously shown that this bacterium triggers host tyrosine kinase-dependent phosphorylation and actin-dependent cytoskeleton reorganization for invasion. On the bacterial side, the leucine-rich repeat cell-surface BspA protein is important for entry. The present study was undertaken to identify host signalling molecules during T. forsythia entry into human oral and cervical epithelial cells. Specifically, the roles of phosphatidylinositol 3-kinase (PI3K), Rho-family GTPases, cholesterol-rich membrane microdomains and the endocytic protein clathrin were investigated. For this purpose, cell lines were pretreated with chemical inhibitors or small interfering RNAs (siRNAs) that target PI3Ks, Rho GTPases, clathrin and cholesterol (a critical component of ‘lipid rafts’), and the resulting effects on T. forsythia uptake were determined. Our studies revealed that T. forsythia entry is dependent on host PI3K signalling, and that purified BspA protein causes activation of this lipid kinase. Bacterial entry also requires the cooperation of host Rac1 GTPase. Finally, our findings indicate an important role for clathrin and cholesterol-rich lipid microdomains in the internalization process

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An In Vitro Model of Ciprofloxacin and Minocycline Transport by Oral Epithelial Cells

Journal of Periodontology ◽

10.1902/jop.2002.73.11.1267 ◽

2002 ◽

Vol 73 (11) ◽

pp. 1267-1272 ◽

Cited By ~ 17

Author(s):

James J. Brayton ◽

Qing Yang ◽

Robin J. Nakkula ◽

John D. Walters

Keyword(s):

Epithelial Cells ◽

In Vitro Model ◽

Oral Epithelial Cells ◽

Vitro Model ◽

Oral Epithelial

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Wild-Type Kaposi's Sarcoma-Associated Herpesvirus Isolated from the Oropharynx of Immune-Competent Individuals Has Tropism for Cultured Oral Epithelial Cells

Journal of Virology ◽

10.1128/jvi.78.8.4074-4084.2004 ◽

2004 ◽

Vol 78 (8) ◽

pp. 4074-4084 ◽

Cited By ~ 48

Author(s):

Karen M. Duus ◽

Vivian Lentchitsky ◽

Timothy Wagenaar ◽

Charles Grose ◽

Jennifer Webster-Cyriaque

Keyword(s):

Epithelial Cells ◽

Neutralizing Antibodies ◽

Kaposi's Sarcoma ◽

Kaposi’S Sarcoma ◽

Wild Type ◽

Oral Epithelial Cells ◽

Kaposi's Sarcoma Associated Herpesvirus ◽

Kaposi’S Sarcoma Associated Herpesvirus ◽

Oral Epithelial

ABSTRACT Based on the observation that wild-type Kaposi's sarcoma-associated herpesvirus (KSHV) DNA can be detected in the oral cavity of healthy, immunocompetent individuals, we hypothesized that epithelial cells could be infected in vitro by wild-type (WT) KSHV isolated from immunocompetent individuals. Primary oral epithelial (P-EPI) cells and telomerase-immortalized oral epithelial cells were generated from human gingival tissue and were then infected in vitro with WT KSHV isolated from throat wash samples. Markers of lytic and latent KSHV infection were detected in cultures by 24 h postinfection by immunofluorescence confocal microscopic assays. The infectivity of the WT and BCBL virus was blocked by neutralizing antibodies against KSHV gB. The presence of KSHV DNA in these cells was confirmed by real-time PCR amplification of different regions of the viral genome. The significant in vitro viral replication that had occurred was inhibited by ganciclovir and by neutralizing antibodies against gB. When infected cultures were examined by scanning electron microscopy, thousands of KSHV particles were clearly visible across the surfaces of P-EPI cells. The detection of enveloped particles indicated that the infectious cycle had proceeded through assembly and egress. We thus demonstrated that oral WT KSHV isolated from immunocompetent individuals was able to infect and replicate in vitro in a relevant primary cell type. Furthermore, our results provide compelling evidence for KSHV transmission within infected oral epithelial cells derived from healthy, immunocompetent populations.

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