scholarly journals Butyrate Decreases ICAM-1 Expression in Human Oral Squamous Cell Carcinoma Cells

2020 ◽  
Vol 21 (5) ◽  
pp. 1679 ◽  
Author(s):  
Gabriel Leonardo Magrin ◽  
Francesca Di Summa ◽  
Franz-Josef Strauss ◽  
Layla Panahipour ◽  
Michael Mildner ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Nuclear Translocation ◽  
Trichostatin A ◽  
Interleukin 1 ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Oral Epithelial Cells ◽  
Oral Squamous Carcinoma ◽  
Oral Epithelial ◽  
The Impact

Short-chain fatty acids (SCFA) are bacterial metabolites that can be found in periodontal pockets. The expression of adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1) within the epithelium pocket is considered to be a key event for the selective transmigration of leucocytes towards the gingival sulcus. However, the impact of SCFA on ICAM-1 expression by oral epithelial cells remains unclear. We therefore exposed the oral squamous carcinoma cell line HSC-2, primary oral epithelial cells and human gingival fibroblasts to SCFA, namely acetate, propionate and butyrate, and stimulated with known inducers of ICAM-1 such as interleukin-1-beta (IL1β) and tumor necrosis factor-alfa (TNFα). We report here that butyrate but not acetate or propionate significantly suppressed the cytokine-induced ICAM-1 expression in HSC-2 epithelial cells and primary epithelial cells. The G-protein coupled receptor-43 (GPR43/ FFAR2) agonist but not the histone deacetylase inhibitor, trichostatin A, mimicked the butyrate effects. Butyrate also attenuated the nuclear translocation of p65 into the nucleus on HSC-2 cells. The decrease of ICAM-1 was independent of Nrf2/HO-1 signaling and phosphorylation of JNK and p38. Nevertheless, butyrate could not reverse an ongoing cytokine-induced ICAM-1 expression in HSC-2 cells. Overall, these observations suggest that butyrate can attenuate cytokine-induced ICAM-1 expression in cells with epithelial origin.

scholarly journals Requirement for Intercellular Adhesion Molecule 1 and Caveolae in Invasion of Human Oral Epithelial Cells by Porphyromonas gingivalis

2005 ◽  
Vol 73 (10) ◽  
pp. 6290-6298 ◽  
Author(s):  
Riyoko Tamai ◽  
Yasuyuki Asai ◽  
Tomohiko Ogawa
Keyword(s):  
Epithelial Cells ◽  
Porphyromonas Gingivalis ◽  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Kb Cells ◽  
Intercellular Adhesion Molecule 1 ◽  
Caveolin 1 ◽  
Oral Epithelial Cells ◽  
Oral Epithelial

ABSTRACT Porphyromonas gingivalis, a periodontopathic bacterium, is known to invade oral epithelial cells in periodontal lesions, although the mechanism is unclear. In the present study, goat polyclonal anti-intercellular adhesion molecule 1 (anti-ICAM-1) antibody inhibited the invasion of P. gingivalis into KB cells (human oral epithelial cells). Further, the P. gingivalis fimbria, a pathogenic adhesion molecule, bound to recombinant human ICAM-1, as shown by enzyme-linked immunosorbent assay. P. gingivalis was also found to colocalize with ICAM-1 on KB cells, as seen with an immunofluorescence microscope, and the knockdown of ICAM-1 in KB cells resulted in the inhibition of P. gingivalis invasion by RNA interference. In addition, methyl-β-cyclodextrin, a cholesterol-binding agent, inhibited the colocalization of P. gingivalis with ICAM-1 and invasion by the microorganism. The colocalization of caveolin-1, a caveolar marker protein, on KB cells with P. gingivalis was also shown, and the knockdown of caveolin-1 in KB cells caused a reduced level of P. gingivalis invasion. These results suggest that ICAM-1 and caveolae are required for the invasion of P. gingivalis into human oral epithelial cells, and these molecules appear to be associated with the primary stages of the development and progression of chronic periodontitis.

Proteolysis of ICAM-1 on Human Oral Epithelial Cells by Gingipains

2003 ◽  
Vol 82 (10) ◽  
pp. 796-801 ◽  
Author(s):  
H. Tada ◽  
S. Sugawara ◽  
E. Nemoto ◽  
T. Imamura ◽  
J. Potempa ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Immune Evasion ◽  
Intercellular Adhesion Molecule ◽  
Dependent Manner ◽  
Intercellular Adhesion Molecule 1 ◽  
Periodontal Tissues ◽  
Oral Epithelial Cells ◽  
Oral Epithelial Cell ◽  
Oral Epithelial

Cysteine proteinases (gingipains) from Porphyromonas gingivalis are considered key virulence factors of severe periodontitis and host immune evasion. Since expression of intercellular adhesion molecule-1 (ICAM-1) on gingival epithelium is indispensable in polymorphonuclear leukocyte (PMN) migration at the site of periodontitis, we examined the effects of gingipains on the expression of ICAM-1 on human oral epithelial cell lines (KB and HSC-2) by flow cytometry and Western blotting. We found that three purified forms of gingipains efficiently reduced ICAM-1 expression on the cells in a time- and dose-dependent manner. Gingipains reduced the expression on fixed cells and degraded the ICAM-1 in the cell membranes, indicating that the reduction resulted from direct proteolysis. They then disturbed the ICAM-1-dependent adhesion of PMNs to the cells. These results indicate that gingipains cleave ICAM-1 on oral epithelial cells, consequently disrupting PMN-oral epithelial cell interaction, and are involved in immune evasion by the bacterium in periodontal tissues.

scholarly journals Behaviour of Human Oral Epithelial Cells Grown on Invisalign® SmartTrack® Material

Materials ◽  
2020 ◽  
Vol 13 (23) ◽  
pp. 5311
Author(s):  
Michael Nemec ◽  
Hans Magnus Bartholomaeus ◽  
Michael H. Bertl ◽  
Christian Behm ◽  
Hassan Ali Shokoohi-Tabrizi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Barrier Function ◽  
Inflammatory Markers ◽  
Cell Counting ◽  
Optical Cell ◽  
Epithelial Barrier Function ◽  
Oral Epithelial Cells ◽  
Oral Epithelial ◽  
The Impact

Invisalign aligners have been widely used to correct malocclusions, but their effect on oral cells is poorly known. Previous research evaluated the impact of aligners’ eluates on various cells, but the cell behavior in direct contact with aligners is not yet studied. In the present study, we seeded oral epithelial cells (cell line Ca9-22) directly on Invisalign SmartTrack material. This material is composed of polyurethane and co-polyester and exhibit better mechanical characteristics compared to the predecessor. Cell morphology and behavior were investigated by scanning electron microscopy and an optical cell moves analyzer. The effect of aligners on cell proliferation/viability was assessed by cell-counting kit (CCK)-8 and 3,4,5-dimethylthiazol-2-yl-2,5-diphenyl tetrazolium bromide (MTT) assay and live/dead staining. The expression of inflammatory markers and proteins involved in epithelial barrier function was measured by qPCR. Cells formed cluster-like structures on aligners. The proliferation/viability of cells growing on aligners was significantly lower (p < 0.05) compared to those growing on tissue culture plastic (TCP). Live/dead staining revealed a rare occurrence of dead cells on aligners. The gene expression level of all inflammatory markers in cells grown on aligners’ surfaces was significantly increased (p < 0.05) compared to cells grown on TCP after two days. Gene expression levels of the proteins involved in barrier function significantly increased (p < 0.05) on aligners’ surfaces after two and seven days of culture. Aligners’ material exhibits no cytotoxic effect on oral epithelial cells, but alters their behavior and the expression of proteins involved in the inflammatory response, and barrier function. The clinical relevance of these effects has still to be established.

scholarly journals Potential Suppressive Effect of Nicotine on the Inflammatory Response in Oral Epithelial Cells: An In Vitro Study

2021 ◽  
Vol 18 (2) ◽  
pp. 483
Author(s):  
Na An ◽  
Jasmin Holl ◽  
Xuekui Wang ◽  
Marco Aoqi Rausch ◽  
Oleh Andrukhov ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Periodontal Diseases ◽  
Suppressive Effect ◽  
Cell Surface Expression ◽  
Epithelial Cell Line ◽  
Oral Epithelial Cells ◽  
Tnf Α ◽  
Oral Epithelial ◽  
The Impact

Smoking is a well-recognized risk factor for oral mucosal and periodontal diseases. Nicotine is an important component of cigarette smoke. This study aims to investigate the impact of nicotine on the viability and inflammatory mediator production of an oral epithelial cell line in the presence of various inflammatory stimuli. Oral epithelial HSC-2 cells were challenged with nicotine (10−8–10−2 M) for 24 h in the presence or absence of Porphyromonas gingivalis lipopolysaccharide (LPS, 1 µg/mL) or tumor necrosis factor (TNF)-α (10−7 M) for 24 h. The cell proliferation/viability was determined by MTT assay. Gene expression of interleukin (IL)-8, intercellular adhesion molecule (ICAM)-1, and β-defensin was assayed by qPCR. The production of IL-8 protein and cell surface expression of ICAM-1 was assessed by ELISA and flow cytometry, respectively. Proliferation/viability of HSC-2 cells was unaffected by nicotine at concentrations up to 10−3 M and inhibited at 10−2 M. Nicotine had no significant effect on the basal expression of IL-8, ICAM-1, and β-defensin. At the same time, it significantly diminished P. gingivalis LPS or the TNF-α-induced expression levels of these factors. Within the limitations of this study, the first evidence was provided in vitro that nicotine probably exerts a suppressive effect on the production of inflammatory mediators and antimicrobial peptides in human oral epithelial cells.

scholarly journals Novel Aggregation Properties of Candida albicans Secreted Aspartyl Proteinase Sap6 Mediate Virulence in Oral Candidiasis

2015 ◽  
Vol 83 (7) ◽  
pp. 2614-2626 ◽  
Author(s):  
Rohitashw Kumar ◽  
Darpan Saraswat ◽  
Swetha Tati ◽  
Mira Edgerton
Keyword(s):  
Candida Albicans ◽  
Epithelial Cells ◽  
Oral Candidiasis ◽  
Oral Microbiome ◽  
Proteinase Activity ◽  
Adhesion Properties ◽  
Content Type ◽  
Oral Epithelial Cells ◽  
Oral Epithelial ◽  
Cell Cell

Candida albicans, a commensal fungus of the oral microbiome, causes oral candidiasis in humans with localized or systemic immune deficiencies. Secreted aspartic proteinases (Saps) are a family of 10 related proteases and are virulence factors due to their proteolytic activity, as well as their roles in adherence and colonization of host tissues. We found that mice infected sublingually withC. albicanscells overexpressing Sap6 (SAP6OE and a Δsap8strain) had thicker fungal plaques and more severe oral infection, while infection with the Δsap6strain was attenuated. These hypervirulent strains had highly aggregative colony structurein vitroand higher secreted proteinase activity; however, the levels of proteinase activity ofC. albicansSaps did not uniformly match their abilities to damage cultured oral epithelial cells (SCC-15 cells). Hyphal induction in cells overexpressing Sap6 (SAP6OE and Δsap8cells) resulted in formation of large cell-cell aggregates. These aggregates could be produced in germinated wild-type cells by addition of native or heat-inactivated Sap6. Sap6 bound only to germinated cells and increasedC. albicansadhesion to oral epithelial cells. The adhesion properties of Sap6 were lost upon deletion of its integrin-binding motif (RGD) and could be inhibited by addition of RGD peptide or anti-integrin antibodies. Thus, Sap6 (but not Sap5) has an alternative novel function in cell-cell aggregation, independent of its proteinase activity, to promote infection and virulence in oral candidiasis.

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