scholarly journals IL-27 Modulates Chemokine Production in TNF-α -Stimulated Human Oral Epithelial Cells

2017 ◽  
Vol 43 (3) ◽  
pp. 1198-1206 ◽  
Author(s):  
Yoshitaka Hosokawa ◽  
Ikuko Hosokawa ◽  
Kazumi Ozaki ◽  
Takashi Matsuo
Keyword(s):  
Signal Transduction ◽  
Epithelial Cells ◽  
Inhibitory Effect ◽  
Chemokine Production ◽  
Oral Epithelial Cells ◽  
Phosphorylation Level ◽  
Stat3 Phosphorylation ◽  
Tnf Α ◽  
Oral Epithelial

Background/Aims: Interleukin-27 (IL-27) is a cytokine which belongs to the IL-12 family. However, the role of IL-27 in the pathogenesis of periodontal disease is uncertain. The aim of this study was to examine the effect of IL-27 on chemokine production in TNF-α-stimulated human oral epithelial cells (TR146). Methods: We measured chemokine production in TR146 by ELISA. We used western blot analysis to detect the phosphorylation levels of signal transduction molecules, including STAT1 and STAT3 in TR146. We used inhibitors to examine the role of STAT1 and STAT3 activation. Results: IL-27 increased CXCR3 ligands production in TNF-α-stimulated TR146. Meanwhile, IL-27 suppressed IL-8 and CCL20 production induced by TNF-α. STAT1 phosphorylation level in IL-27 and TNF-α-stimulated TR146 was enhanced in comparison to TNF-α-stimulated TR146. STAT3 phosphorylation level in IL-27-treated TR146 did not change by TNF-α. Both STAT1 inhibitor and STAT3 inhibitor decreased CXCR3 ligands production. STAT1 inhibitor overrode the inhibitory effect of IL-27 on IL-8 and CCL20 production in TNF-α-stimulated TR146. Meanwhile, STAT3 inhibitor did not modulate IL-8 and CCL20 production. Conclusion: IL-27 might control leukocyte migration in periodontal lesion by modulating chemokine production from epithelial cells.

scholarly journals Immune Tolerance in the Oral Mucosa

2021 ◽  
Vol 22 (22) ◽  
pp. 12149
Author(s):  
Hector F. Pelaez-Prestel ◽  
Jose L. Sanchez-Trincado ◽  
Esther M. Lafuente ◽  
Pedro A. Reche
Keyword(s):  
Epithelial Cells ◽  
Oral Mucosa ◽  
Immune Cells ◽  
Commensal Bacteria ◽  
First Line ◽  
Innate And Adaptive Immunity ◽  
Oral Epithelial Cells ◽  
A Site ◽  
Oral Epithelial

The oral mucosa is a site of intense immune activity, where a large variety of immune cells meet to provide a first line of defense against pathogenic organisms. Interestingly, the oral mucosa is exposed to a plethora of antigens from food and commensal bacteria that must be tolerated. The mechanisms that enable this tolerance are not yet fully defined. Many works have focused on active immune mechanisms involving dendritic and regulatory T cells. However, epithelial cells also make a major contribution to tolerance by influencing both innate and adaptive immunity. Therefore, the tolerogenic mechanisms concurring in the oral mucosa are intertwined. Here, we review them systematically, paying special attention to the role of oral epithelial cells.

scholarly journals Potential role of high molecular weight hyaluronan in the anti-Candidaactivity of human oral epithelial cells

2007 ◽  
Vol 45 (1) ◽  
pp. 73-79 ◽  
Author(s):  
Akiyoshi Sakai ◽  
Sumio Akifusa ◽  
Naoki Itano ◽  
Koji Kimata ◽  
Taro Kawamura ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Epithelial Cells ◽  
High Molecular Weight ◽  
Potential Role ◽  
Oral Epithelial Cells ◽  
Oral Epithelial

scholarly journals Role of OmpA2 surface regions ofPorphyromonas gingivalisin host-pathogen interactions with oral epithelial cells

2016 ◽  
Vol 6 (1) ◽  
pp. e00401 ◽  
Author(s):  
Kathryn L. Naylor ◽  
Magdalena Widziolek ◽  
Stuart Hunt ◽  
Mary Conolly ◽  
Matthew Hicks ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Host Pathogen Interactions ◽  
Oral Epithelial Cells ◽  
Host Pathogen ◽  
Oral Epithelial

The role of phosphoinositide 3-kinase in adhesion of oral epithelial cells to titanium

2013 ◽  
Vol 58 (11) ◽  
pp. 1696-1708 ◽  
Author(s):  
Ikiru Atsuta ◽  
Yasunori Ayukawa ◽  
Takayoshi Yamaza ◽  
Akihiro Furuhashi ◽  
Kiyoshi Koyano
Keyword(s):  
Epithelial Cells ◽  
Oral Epithelial Cells ◽  
Phosphoinositide 3 Kinase ◽  
Oral Epithelial

IL-29 Enhances CXCL10 Production in TNF-α-stimulated Human Oral Epithelial Cells

2017 ◽  
Vol 46 (6) ◽  
pp. 615-624 ◽  
Author(s):  
Yoshitaka Hosokawa ◽  
Ikuko Hosokawa ◽  
Satoru Shindo ◽  
Kazumi Ozaki ◽  
Takashi Matsuo
Keyword(s):  
Epithelial Cells ◽  
Oral Epithelial Cells ◽  
Tnf Α ◽  
Oral Epithelial

Potential role of Candida albicans secreted aspartic protease 9 in serum induced-hyphal formation and interaction with oral epithelial cells

2020 ◽  
Vol 139 ◽  
pp. 103896
Author(s):  
Haiping Yang ◽  
Peter Chiu Shun Tsang ◽  
Edmond Ho Nang Pow ◽  
Otto Lok Tao Lam ◽  
Paul Wai-Kei Tsang
Keyword(s):  
Candida Albicans ◽  
Epithelial Cells ◽  
Potential Role ◽  
Aspartic Protease ◽  
Oral Epithelial Cells ◽  
Hyphal Formation ◽  
Oral Epithelial

Cigarette smoking promotes cancer-related transformation of oral epithelial cells through activation of Wnt and MAPK pathway

2019 ◽  
Vol 15 (31) ◽  
pp. 3619-3631
Author(s):  
Ripon Sarkar ◽  
Ankita Das ◽  
Ranjan R Paul ◽  
Ananya Barui
Keyword(s):  
Epithelial Cells ◽  
Cigarette Smoking ◽  
Mapk Pathway ◽  
Mrna Level ◽  
Real Time Quantitative Pcr ◽  
Oral Epithelial Cells ◽  
Mapk Pathways ◽  
Tnf Α ◽  
Canonical Wnt ◽  
Oral Epithelial

Aim: Study aims to investigate the effect of cigarette smoking on cancer-related transformation in oral epithelial cells of smokers through evaluating the alteration in Wnt/β-catenin and MAPK pathways. Materials & methods: Exfoliated oral epithelial cells were collected from 138 subjects and categorized into nonsmokers, smokers and clinically diagnosed precancer and cancer patients. Real-time quantitative PCR was performed to detect the fold changes of related genes. Expressions of biomarkers were assessed using immunofluorescence and western blot. Results: Study shows significant (p < 0.001) alteration in mRNA level of TNF-α, NF-κβ, FZD1, β-catenin, PARD 3, MAPK1 and vimentin genes under cigarette smoking. Conclusion: Results suggested the progression of oral cancer under cigarette smoking occurs through multiple events and activation of canonical Wnt/MAPK pathways.

scholarly journals Reduced Salivary Mucin Binding and Glycosylation in Older Adults Influences Taste in an In Vitro Cell Model

Nutrients ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 2280 ◽  
Author(s):  
Rose-Anna G. Pushpass ◽  
Nicola Pellicciotta ◽  
Charles Kelly ◽  
Gordon Proctor ◽  
Guy H. Carpenter
Keyword(s):  
Older Adults ◽  
Epithelial Cells ◽  
Taste Receptor ◽  
Receptor Activation ◽  
Oral Epithelium ◽  
Younger Adults ◽  
Oral Epithelial Cells ◽  
Salivary Mucin ◽  
Oral Epithelial

Background: Taste loss is a significant problem in older adults, affecting quality of life and nutrition. Altered salivary rheology and loss of mucin function may contribute to taste loss by reducing mucosal defences in the oral cavity, impairing sensitivity to oral stimulants. This study aimed to investigate the effects of salivary rheology on taste loss in ageing. Salivary mucin glycosylation and binding to the oral epithelium was investigated in older and younger adults. A cell-based model was utilised to consider the role of saliva in taste loss. Methods: Human subjects aged >60 years (n = 25) and 18–30 (n = 30) provided saliva samples which were analysed for viscosity, mucin composition and mucin binding to oral epithelial cells (TR146/MUC1). Oral epithelial cells (TR146/MUC1 and SCC090) provided models for taste receptor activation. Results: Reduced levels and sialylation of MUC7 were evident in saliva of older adults which may lead to reduced viscoelasticity, while viscosity is unaffected. Impaired muco-adhesion of saliva from older adults was also observed. Saliva from older adults facilitated the bitter taste receptor activation less well than saliva from younger adults. The causes of taste dysfunction in older adults are unknown, but this study supports a role of saliva in facilitating the activation of taste receptors.

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