scholarly journals Role of Porphyromonas gingivalis SerB in Gingival Epithelial Cell Cytoskeletal Remodeling and Cytokine Production

2008 ◽  
Vol 76 (6) ◽  
pp. 2420-2427 ◽  
Author(s):  
Yoshiaki Hasegawa ◽  
Gena D. Tribble ◽  
Henry V. Baker ◽  
Jeffrey J. Mans ◽  
Martin Handfield ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Actin Cytoskeleton ◽  
Porphyromonas Gingivalis ◽  
Cytokine Production ◽  
Critical Role ◽  
Fusobacterium Nucleatum ◽  
Transcriptional Profile ◽  
Cytoskeletal Remodeling ◽  
Gingival Epithelial Cell ◽  
Gingival Epithelial Cells

ABSTRACT The SerB protein of Porphyromonas gingivalis is a HAD family serine phosphatase that plays a critical role in entry and survival of the organism in gingival epithelial cells. SerB is secreted by P. gingivalis upon contact with epithelial cells. Here it is shown by microarray analysis that SerB impacts the transcriptional profile of gingival epithelial cells, with pathways involving the actin cytoskeleton and cytokine production among those significantly overpopulated with differentially regulated genes. Consistent with the transcriptional profile, a SerB mutant of P. gingivalis exhibited defective remodeling of actin in epithelial cells. Interaction between gingival epithelial cells and isolated SerB protein resulted in actin rearrangement and an increase in the F/G actin ratio. SerB protein was also required for P. gingivalis to antagonize interleukin-8 accumulation following stimulation of epithelial cells with Fusobacterium nucleatum. SerB is thus capable of modulating host cell signal transduction that impacts the actin cytoskeleton and cytokine production.

scholarly journals Role of Porphyromonas gingivalis Phosphoserine Phosphatase Enzyme SerB in Inflammation, Immune Response, and Induction of Alveolar Bone Resorption in Rats

2010 ◽  
Vol 78 (11) ◽  
pp. 4560-4569 ◽  
Author(s):  
Brian Bainbridge ◽  
Raj K. Verma ◽  
Christie Eastman ◽  
Bilal Yehia ◽  
Mercedes Rivera ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Epithelial Cells ◽  
Periodontal Disease ◽  
Porphyromonas Gingivalis ◽  
Rat Model ◽  
Alveolar Bone ◽  
Critical Role ◽  
Polymorphonuclear Neutrophil ◽  
Gingival Epithelial Cells ◽  
Phosphatase Enzyme

ABSTRACT Porphyromonas gingivalis secretes a serine phosphatase enzyme, SerB, upon contact with gingival epithelial cells in vitro. The SerB protein plays a critical role in internalization and survival of the organism in epithelial cells. SerB is also responsible for the inhibition of interleukin-8 (IL-8) secretion from gingival epithelial cells infected with P. gingivalis. This study examined the ability of a P. gingivalis SerB mutant to colonize the oral cavity and induce gingival inflammation, immune responses, and alveolar bone resorption in a rat model of periodontal disease. Both P. gingivalis ATCC 33277 and an isogenic ΔSerB mutant colonized the oral cavities of rats during the 12-week experimental period. Both of the strains induced significant (P < 0.05) systemic levels of immunoglobulin G (IgG) and isotypes IgG1, IgG2a, and IgG2b, indicating the involvement of both T helper type 1 (Th1) and Th2 responses to infection. Both strains induced significantly (P < 0.05) higher levels of alveolar bone resorption in infected rats than in sham-infected control rats. However, horizontal and interproximal alveolar bone resorption induced by the SerB mutant was significantly (P < 0.05) lower than that induced by the parental strain. Rats infected with the ΔSerB mutant exhibited significantly higher levels of apical migration of the junctional epithelium (P < 0.01) and polymorphonuclear neutrophil (PMN) recruitment (P < 0.001) into the gingival tissues than rats infected with the wild type. In conclusion, in a rat model of periodontal disease, the SerB phosphatase of P. gingivalis is required for maximal alveolar bone resorption, and in the absence of SerB, more PMNs are recruited into the gingival tissues.

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.

scholarly journals Porphyromonas gingivalis entry into gingival epithelial cells modulated by Fusobacterium nucleatum is dependent on lipid rafts

2012 ◽  
Vol 53 (5-6) ◽  
pp. 234-242 ◽  
Author(s):  
Atsushi Saito ◽  
Eitoyo Kokubu ◽  
Satoru Inagaki ◽  
Kentaro Imamura ◽  
Daichi Kita ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Lipid Rafts ◽  
Porphyromonas Gingivalis ◽  
Fusobacterium Nucleatum ◽  
Gingival Epithelial Cells

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.

Sign in / Sign up

Export Citation Format

Share Document