Irsogladine maleate inhibits Porphyromonas gingivalis -mediated expression of toll-like receptor 2 and interleukin-8 in human gingival epithelial cells

2014 ◽  
Vol 50 (4) ◽  
pp. 486-493 ◽  
Author(s):  
I. J. Savitri ◽  
K. Ouhara ◽  
T. Fujita ◽  
M. Kajiya ◽  
T. Miyagawa ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Porphyromonas Gingivalis ◽  
Interleukin 8 ◽  
Toll Like Receptor ◽  
Irsogladine Maleate ◽  
Gingival Epithelial Cells ◽  
Toll Like Receptor 2 ◽  
Human Gingival Epithelial Cells

scholarly journals Toll-Like Receptor 2-Mediated Interleukin-8 Expression in Gingival Epithelial Cells by the Tannerella forsythia Leucine-Rich Repeat Protein BspA

2007 ◽  
Vol 76 (1) ◽  
pp. 198-205 ◽  
Author(s):  
Shinsuke Onishi ◽  
Kiyonobu Honma ◽  
Shuang Liang ◽  
Panagiota Stathopoulou ◽  
Denis Kinane ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Interleukin 8 ◽  
Host Cells ◽  
Leucine Rich Repeat ◽  
Toll Like Receptor ◽  
Periodontal Pathogens ◽  
Tannerella Forsythia ◽  
Multifunctional Protein ◽  
Gingival Epithelial Cells ◽  
Human Gingival Epithelial Cells

ABSTRACT Tannerella forsythia is a gram-negative anaerobe strongly associated with chronic human periodontitis. This bacterium expresses a cell surface-associated and secreted protein, designated BspA, which has been recognized as an important virulence factor. The BspA protein belongs to the leucine-rich repeat (LRR) and bacterial immunoglobulin-like protein families. BspA is, moreover, a multifunctional protein which interacts with a variety of host cells, including monocytes which appear to respond to BspA through Toll-like receptor (TLR) signaling. Since gingival epithelium forms a barrier against periodontal pathogens, this study was undertaken to determine if gingival epithelial cells respond to BspA challenge and if TLRs play any role in BspA recognition. This study was also directed towards identifying the BspA domains responsible for cellular activation. We provide direct evidence for BspA binding to TLR2 and demonstrate that the release of the chemokine interleukin-8 from human gingival epithelial cells by BspA is TLR2 dependent. Furthermore, the LRR domain of BspA is involved in activation of TLR2, while TLR1 serves as a signaling partner. Thus, our findings suggest that BspA is an important modulator of host innate immune responses through activation of TLR2 in cooperation with TLR1.

scholarly journals Oral Treponemes and Their Outer Membrane Extracts Activate Human Gingival Epithelial Cells through Toll-Like Receptor 2

2003 ◽  
Vol 71 (2) ◽  
pp. 717-725 ◽  
Author(s):  
Yasuyuki Asai ◽  
Takayoshi Jinno ◽  
Tomohiko Ogawa
Keyword(s):  
Monoclonal Antibody ◽  
Epithelial Cells ◽  
Mrna Expression ◽  
Outer Membrane ◽  
Periodontal Diseases ◽  
Treponema Denticola ◽  
Toll Like Receptor ◽  
Gingival Epithelial Cells ◽  
Toll Like Receptor 2 ◽  
Human Gingival Epithelial Cells

ABSTRACT Oral treponemes are considered to be important in the development and progression of periodontal diseases. We investigated the mechanisms of recognition and activation of human gingival epithelial cells (HGEC) with the oral treponemes Treponema denticola, Treponema vincentii, and Treponema medium and their outer membrane extracts (OMEs). T. vincentii and T. medium but not T. denticola produced interleukin 8 (IL-8) in an HGEC culture. Further, all three treponemes induced IL-8 mRNA expression and NF-κB activation in HGEC. Among them, T. denticola especially exhibited trypsin- and chymotrypsin-like protease activities, and the addition of chymostatin, a chymotrypsin protease inhibitor, resulted in detectable IL-8 production by HGEC cultured with T. denticola. Additionally, IL-8 mRNA expression in HGEC cultured with the three treponemes and their OMEs was definitely inhibited by the mouse anti-human Toll-like receptor 2 (TLR2) monoclonal antibody TL2.1. These findings suggest that oral treponemes and their OMEs activate HGEC through TLR2.

scholarly journals Treponema denticola Suppresses Expression of Human β-Defensin-3 in Gingival Epithelial Cells through Inhibition of the Toll-Like Receptor 2 Axis

2009 ◽  
Vol 78 (2) ◽  
pp. 672-679 ◽  
Author(s):  
Ji Eun Shin ◽  
Young Sook Kim ◽  
Ju-Eun Oh ◽  
Byung-Moo Min ◽  
Youngnim Choi
Keyword(s):  
Epithelial Cells ◽  
Suppressive Effect ◽  
Inhibitory Effect ◽  
Mitogen Activated Protein Kinase ◽  
Treponema Denticola ◽  
Toll Like Receptor ◽  
Periodontal Pathogens ◽  
Gingival Epithelial Cells ◽  
Toll Like Receptor 2 ◽  
Human Gingival Epithelial Cells

ABSTRACT We reported previously that Treponema denticola, one of the periodontal pathogens, suppresses the expression of human β-defensins (HBDs) in human gingival epithelial cells. To identify the mechanisms involved in this suppression, immortalized and normal human gingival epithelial cells were infected with live or heat-killed T. denticola for 24 h, and then the expression of HBDs was examined by real-time RT-PCR. Live T. denticola suppressed the expression of HBD-3 substantially and also suppressed the expression of HBD-1 and HBD-2. However, heat-killed bacteria did not produce a suppressive effect but instead slightly upregulated the levels of HBD-2 and HBD-3. In contrast to live T. denticola, which reduced the activation of mitogen-activated protein kinase (MAPK) and NF-κB within an hour of infection, heat-killed bacteria did not show any inhibitory effect on the MAPK and NF-κB signaling pathways. Knockdown of Toll-like receptor 2 (TLR2) via RNA interference abolished the suppressive effect of T. denticola on the expression of HBD-3. Heat-killed T. denticola but not live bacteria could activate TLR2 in CHO/CD14/TLR2 reporter cells, suggesting that T. denticola contains a heat-labile inhibitor(s) of TLR2 in addition to ligands recognized by TLR2. Indeed, live T. denticola was able to inhibit TLR2 activation by Pam3CSK. In conclusion, T. denticola suppressed the expression of HBD-3 by inhibiting the TLR2 axis in gingival epithelial cells. These results may provide new insight into the pathogenesis of periodontitis caused by T. denticola.

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

2004 ◽  
Vol 72 (7) ◽  
pp. 3752-3758 ◽  
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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