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Effect of P. gingivalis on human primary gingival epithelial cells

ABSTRACT: EXPERIMENT: Microarray expression profiles derived from the human primary gingival epithelial cells 24.0h after exposure to heat inactivated P. gingivalis ANIMAL MODEL: NON EXPOSURE: Human primary gingival epithelial cells (at 3rd passage) were exposed to heat inactivated P. gingivalis (MOI:100) at 90% confluence. Two types of gingival epithelial cells were used. One with Normal cytokine inducer type (at least 2 fold IL-6/TNF-alpha/IL-1ß when challenged with TLR2/4 agonists) and the other with diminished cytokine inducer type (no change in IL-6/TNF-alpha/IL-1ß when challenged with TLR2/4 agonists). INTERVAL: NON. PLATFORM: microRNA expression profile in gingival epithelial cells - miRCURY LNA™ microRNA Arrays (Exiqon). The RNA samples were subjected to microarray on 8/9/2007 Keywords = Human primary gingival epithelial cells Keywords = P. gingivalis Keywords = Periodontitis Keywords: Ordered

ORGANISM(S): Homo sapiens

PROVIDER: GSE13042 | GEO | 2008/11/07

SECONDARY ACCESSION(S): PRJNA109951

REPOSITORIES: GEO

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Effect of P. gingivalis on human primary gingival epithelial cells

Project description:EXPERIMENT: Microarray expression profiles derived from the human primary gingival epithelial cells 24.0h after exposure to heat inactivated P. gingivalis ANIMAL MODEL: NON EXPOSURE: Human primary gingival epithelial cells (at 3rd passage) were exposed to heat inactivated P. gingivalis (MOI:100) at 90% confluence. Two types of gingival epithelial cells were used. One with Normal cytokine inducer type (at least 2 fold IL-6/TNF-alpha/IL-1Ã when challenged with TLR2/4 agonists) and the other with diminished cytokine inducer type (no change in IL-6/TNF-alpha/IL-1Ã when challenged with TLR2/4 agonists). INTERVAL: NON. PLATFORM: microRNA expression profile in gingival epithelial cells - miRCURY LNAâ¢ microRNA Arrays (Exiqon). The RNA samples were subjected to microarray on 8/9/2007 Keywords = Human primary gingival epithelial cells Keywords = P. gingivalis Keywords = Periodontitis Keywords: Ordered The effect of heat inactivated P. gingivalison human primary gingival epithelial cells were assayed.

2010-05-16 | E-GEOD-13042 | biostudies-arrayexpress

Explore the gene expression files of HGECs after P. gingivalis persisters treatment via RNA sequencing

Project description:This study investigated how P. gingivalis persisters interacted with human gingival epithelial cells (HGECs) and affected the gene expression of cytokines, and the related signaling pathways, via RNA sequencing. P. gingivalis (ATCC 33277) was treated with metronidazole (100 μg/ml) for 6 hours to generate P. gingivalis persisters (M-PgPs). HGECs with or without IL-1β pretreatment were stimulated by M-PgPs and P. gingivalis for 24 hours, and those without any treatments served as the blank control (BL).

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Differential protein expression by Porphyromonas gingivalis in response to secreted epithelial cell components

Project description:The human oral pathogen Porphyromonas gingivalis colonizes the gingival crevice and invades gingival epithelial cells. Multidimensional capillary high-performance liquid chromatography coupled with tandem mass spectrometry and two-dimensional gel electrophoresis were used to analyze the proteome of P. gingivalis as it adapts to a set of experimental conditions designed to reflect important features of an epithelial cell environment. 1014 proteins (46% of the total theoretical proteome) were identified in four independent analyses; 479 of these proteins showed evidence of differential expression after exposure of P. gingivalis to either conditioned epithelial cell growth medium or control conditions: i.e., they were only detected under one set of conditions. Moreover, 276 genes annotated as hypothetical were found to encode expressed proteins. Among the proteins up-regulated in the presence of epithelial cell components were a homolog of the internalin proteins of Listeria monocytogenes and subunits of the ATP-dependent Clp protease complex. Insertional inactivation of clpP, encoding the Clp proteolytic subunit, resulted in approximately a 50% reduction in invasion of P. gingivalis. These results suggest that adaptation to an epithelial cell environment induces a major shift in the expressed proteome of the organism. Furthermore, ClpP, that is up-regulated in this environment, is required for optimal invasive activity of P. gingivalis. Keywords: proteome analysis of P. gingivalis

2005-09-17 | GSE3322 | GEO

Gingival Epithelial Cell Transcriptional Responses to Pathogenic Oral Microbial Species.

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Transcription profiling of human gingival epithelial cells responses to pathogenic oral microbial species.

Project description:Transcriptional profiling was utilized to define the biological pathways of gingival epithelial cells modulated by co-culture with the oral pathogenic Porphyromonas gingivalis and Aggregatibacter (formerly actinobacillus) actinomycetemcomitans. We used microarrays to detail the global programme of gene expression underlying infection and identified distinct classes of up- and down-regulated genes during this process. Experiment Overall Design: Gingival epithelial HIGK cells were sham infected (CTRL) and infected with either the oral pathogenic P. gingivalis (Pg) or A. actinomycetemcomitans (Aa). These samples were hybridized to Affymetrix microarrays. Understanding how host cells have adapted to pathogens, and how barrier cells respond to limit their impact, provides a mechanistic biological basis of microbial disease in the mixed bacterial-human ecosystem of the oral cavity.

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membrane substrates of gingipains

Project description:Porphyromonas gingivalis secretes cysteine proteases named gingipains which can cleave an array of proteins and importantly contribute to the development of periodontitis. In this study we focused on gingipain-exerted proteolysis at the cell surface of human gingival epithelial cells (telomerase immortalized gingival keratinocytes [TIGK]). We examined whether gingipains have sheddase activity or if their main activity is degradation of membrane proteins into small fragments. Using mass spectrometry, we investigated the whole sheddome/degradome of TIGK cell surface proteins by P. gingivalis strains differing in gingipain expression. We observed extensive degradation of TIGK surface proteins, suggesting that gingipains could in fact be the major cause of damage to the gingival epithelium. Most of the identified gingipain substrates were molecules involved in adhesion, suggesting that gingipains may cause tissue damage through cleavage of cell contacts, resulting in cell detachment and rounding, and consequently leading to anoikis. These results reveal a molecular underpinning to P. gingivalis-induced tissue destruction and enhance our knowledge of the role of P. gingivalis’ proteases in the pathobiology of periodontitis.

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Transcription profiling of human oral keratinocytes was utilized to define the biological role of P. gingivalis in gingival epithelial cell cytoskeletal remodeling and cytokine production

Project description:Transcriptional profiling of oral keratinocytes was utilized to define the biological role of P. gingivalis SerB. We used microarrays to detail the global programme of gene expression underlying infection with an isogenic mutant in SerB, and identified distinct classes of up- and down-regulated genes during this process. Experiment Overall Design: Gingival epithelial HIGK cells were infected with either the oral pathogen P. gingivalis (Pg) or an isogenic mutant for SerB in the same parental strain in order to gain a better understanding on the role of SerB. These samples were hybridized to Affymetrix microarrays. SerB was found to be a multifunctional invasin and modulin of P. gingivalis and associated with broadly based regulation of the epithelial cell transcriptome.

2008-06-18 | E-GEOD-10526 | biostudies-arrayexpress

Transcription profiling by array of human gingival epithelial cell responses to a complex microbiome

Project description:Transcriptional profiling was utilized to define the biological pathways of gingival epithelial cells modulated by mono- and complex co-culture with oral commensal S. gordonii and pathogenic P. gingivalis. We used microarrays to detail the global programme of gene expression underlying infection and identified distinct classes of up- and down-regulated genes during this process. Experiment Overall Design: Gingival epithelial HIGK cells were sham infected (CTRL) and infected with either the oral commensal S. gordonii (Sg) or the pathogenic P. gingivalis (Pg) as well as co-cultured in mixed cultures of Sg and Pg (Sg+Pg). These samples were hybridized to Affymetrix microarrays. Understanding how host cells have adapted to commensals, and how barrier cells respond to limit their impact, provides a mechanistic biological basis of health in the mixed bacterial-human ecosystem of the oral cavity and provides insight on how the degree of complexity of a microbiome influences this balance.

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