scholarly journals In Vitro Effects of Streptococcus oralis Biofilm on Peri-Implant Soft Tissue Cells

Cells ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 1226
Author(s):  
Alexandra Ingendoh-Tsakmakidis ◽  
Jörg Eberhard ◽  
Christine S. Falk ◽  
Meike Stiesch ◽  
Andreas Winkel
Keyword(s):  
Soft Tissue ◽  
Stress Responses ◽  
Cell Types ◽  
Cellular Damage ◽  
Streptococcus Oralis ◽  
Gingival Epithelial Cells ◽  
Tissue Cells ◽  
In Vitro Effects ◽  
Human Gingival Epithelial Cells

Human gingival epithelial cells (HGEps) and fibroblasts (HGFs) are the main cell types in peri-implant soft tissue. HGEps are constantly exposed to bacteria, but HGFs are protected by connective tissue as long as the mucosa–implant seal is intact. Streptococcus oralis is one of the commensal bacteria, is highly abundant at healthy implant sites, and might modulate soft tissue cells—as has been described for other streptococci. We have therefore investigated the effects of the S. oralis biofilm on HGEps and HGFs. HGEps or HGFs were grown separately on titanium disks and responded to challenge with S. oralis biofilm. HGFs were severely damaged after 4 h, exhibiting transcriptional inflammatory and stress responses. In contrast, challenge with S. oralis only induced a mild transcriptional inflammatory response in HGEps, without cellular damage. HGFs were more susceptible to the S. oralis biofilm than HGEps. The pro-inflammatory interleukin 6 (IL-6) was attenuated in HGFs, as was interleukin 8 (CXCL8) in HGEps. This indicates that S. oralis can actively protect tissue. In conclusion, commensal biofilms can promote homeostatic tissue protection, but only if the implant–mucosa interface is intact and HGFs are not directly exposed.

Biocompatibility testing of an experimental fluoride releasing resin using human gingival epithelial cells in vitro

1989 ◽  
Vol 25 (1) ◽  
pp. 57-62 ◽  
Author(s):  
Frederick H. Kasten ◽  
L. Fatima R. Pineda ◽  
Paul E. Schneider ◽  
H. Ralph Rawls ◽  
Theda A. Foster
Keyword(s):  
Epithelial Cells ◽  
Gingival Epithelial Cells ◽  
Biocompatibility Testing ◽  
Human Gingival Epithelial Cells

Effect of Inflammation on the Proliferation of Human Gingival Epithelial Cells In Vitro

1997 ◽  
Vol 68 (11) ◽  
pp. 1070-1075 ◽  
Author(s):  
Odile M. Carro ◽  
Suvia A. S. Evans ◽  
Cataldo W. Leone
Keyword(s):  
Epithelial Cells ◽  
Gingival Epithelial Cells ◽  
Human Gingival Epithelial Cells

CC chemokine receptor 5 gene promoter activation by the cyclic AMP response element binding transcription factor

Blood ◽  
2008 ◽  
Vol 112 (5) ◽  
pp. 1610-1619 ◽  
Author(s):  
Hedwich F. Kuipers ◽  
Paula J. Biesta ◽  
Lisette J. Montagne ◽  
Elise S. van Haastert ◽  
Paul van der Valk ◽  
...  
Keyword(s):  
Chemokine Receptor ◽  
Stress Responses ◽  
Inflammatory Diseases ◽  
Transplant Rejection ◽  
Cell Types ◽  
In Vitro Assays ◽  
Specific Expression ◽  
Mhc Molecules ◽  
Creb Pathway

Abstract The chemokine receptor CCR5 is implicated in the pathogenesis of various inflammatory diseases, such as multiple sclerosis (MS), atherosclerosis, transplant rejection, and autoimmunity. In previous studies, we have shown that MS lesions are characterized by enhanced expression of transcription factors associated with stress responses, ie, IRF-1, NF-κB, and CREB-1, which modulate expression of both classes of major histocompatibility complex (MHC) molecules. The expression of MHC-I and MHC-II molecules greatly overlaps with the expression of CCR5 in MS lesions. Therefore, we investigated whether these factors are also involved in the transcriptional regulation of CCR5. Using in vitro assays, we determined that neither IRF-1 nor NF-κB is involved in the activation of the CCR5 promoter. This is corroborated by the finding that these factors are not involved in the induction of endogenous CCR5 transcription in various cell types. In contrast, we show that CCR5 expression is regulated by the cAMP/CREB pathway and that interference in this pathway affects endogenous CCR5 transcription. From this, we conclude that the cAMP/CREB pathway is involved in the regulation of CCR5 transcription and that, given the ubiquitous nature of CREB-1 protein expression, additional regulatory mechanisms must contribute to cell type-specific expression of CCR5.

scholarly journals Staphylococcus aureus Extracellular Vesicles: A Story of Toxicity and the Stress of 2020

Toxins ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 75
Author(s):  
Xiaogang Wang ◽  
Paul F. Koffi ◽  
Olivia F. English ◽  
Jean C. Lee
Keyword(s):  
Staphylococcus Aureus ◽  
Extracellular Vesicles ◽  
Stress Responses ◽  
Cell Types ◽  
Biologically Active ◽  
Host Cells ◽  
Virulence Determinants ◽  
Subinhibitory Concentrations ◽  
Secretory System

Staphylococcus aureus generates and releases extracellular vesicles (EVs) that package cytosolic, cell-wall associated, and membrane proteins, as well as glycopolymers and exoproteins, including alpha hemolysin, leukocidins, phenol-soluble modulins, superantigens, and enzymes. S. aureus EVs, but not EVs from pore-forming toxin-deficient strains, were cytolytic for a variety of mammalian cell types, but EV internalization was not essential for cytotoxicity. Because S. aureus is subject to various environmental stresses during its encounters with the host during infection, we assessed how these exposures affected EV production in vitro. Staphylococci grown at 37 °C or 40 °C did not differ in EV production, but cultures incubated at 30 °C yielded more EVs when grown to the same optical density. S. aureus cultivated in the presence of oxidative stress, in iron-limited media, or with subinhibitory concentrations of ethanol, showed greater EV production as determined by protein yield and quantitative immunoblots. In contrast, hyperosmotic stress or subinhibitory concentrations of erythromycin reduced S. aureus EV yield. EVs represent a novel S. aureus secretory system that is affected by a variety of stress responses and allows the delivery of biologically active pore-forming toxins and other virulence determinants to host cells.

scholarly journals Differential Activation of Human Gingival Epithelial Cells and Monocytes by Porphyromonas gingivalis Fimbriae

2006 ◽  
Vol 75 (2) ◽  
pp. 892-898 ◽  
Author(s):  
Mehmet A. Eskan ◽  
George Hajishengallis ◽  
Denis F. Kinane
Keyword(s):  
Epithelial Cells ◽  
Porphyromonas Gingivalis ◽  
Cell Types ◽  
Induced Response ◽  
Soluble Cd14 ◽  
Necrosis Factor Alpha ◽  
Gingival Epithelial Cell ◽  
Gingival Epithelial Cells ◽  
Macrophage Colony ◽  
Human Gingival Epithelial Cells

ABSTRACT Humans develop periodontitis in response to challenge by microbial dental plaque. Inflammation begins after perturbation of gingival epithelial cells by subgingival bacteria interacting through pattern-recognition receptors, including the Toll-like receptors (TLR). Porphyromonas gingivalis is a major periodontopathogen that interacts with epithelial cells through its cell surface fimbriae (FimA), leading to colonization and/or invasion. Previous work by our group has established membrane CD14 as an essential coreceptor for TLR2-mediated activation of transfected cell lines by P. gingivalis FimA. We have shown that gingival epithelial cells express TLR2 but not CD14 on their cell surfaces. We thus speculated that P. gingivalis FimA does not readily activate epithelial innate immune responses but rather functions to promote P. gingivalis colonization in the absence of a vigorous FimA-induced response. This hypothesis was verified by the findings that primary human gingival epithelial cells responded poorly to FimA in terms of interleukin (IL)-6, IL-8, granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor alpha responses, in stark contrast to the marked response to other TLR2 agonists (Pam3Cys, FSL-1) that are not strictly dependent on CD14. On the other hand, CD14-expressing human primary monocytes responded with high levels of the same cytokines to both FimA and the control TLR2 agonists. The gingival epithelial cells failed to respond to FimA even in the presence of exogenously added soluble CD14. These data indicate that the gingival epithelial cell hyporesponsiveness to FimA is attributable to the lack of membrane-expressed but not soluble CD14. In conclusion, P. gingivalis FimA differentially activates human monocytes and epithelial cells, perhaps reflecting different tactics used by P. gingivalis when interacting with different host cell types or a host strategy to limit inflammation.

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