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Gingival Epithelial Cell Responses to a Complex Microbiome Comprising Commensal and Opportunistic Oral Microbial Species

ABSTRACT: 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. Keywords: infection state

ORGANISM(S): Homo sapiens

PROVIDER: GSE12121 | GEO | 2009/07/14

SECONDARY ACCESSION(S): PRJNA113779

REPOSITORIES: GEO

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Gingival Epithelial Cell Transcriptional Responses to Commensal and Opportunistic Oral Microbial Species.

2007-06-21 | GSE6927 | GEO

Transcription profiling of human gingival epithelial cell transcriptional responses to commensal and opportunistic 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 commensal S. gordonii and the opportunistic commensal F. nucleatum. 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 opportunistic commensal F. nucleatum (Fn). 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.

2009-04-28 | E-GEOD-6927 | 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.

2009-07-18 | E-GEOD-12121 | biostudies-arrayexpress

Gingival Epithelial Cell Transcriptional Responses to Pathogenic Oral Microbial Species.

2008-03-01 | GSE9723 | GEO

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.

2009-04-24 | E-GEOD-9723 | biostudies-arrayexpress

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-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

2008-11-07 | GSE13042 | GEO

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

Gingival epithelial cell transcriptional responses to commensal and opportunistic oral microbial species.

Project description:Transcriptional profiling and ontology tools were utilized to define the biological pathways of gingival epithelial cells modulated by coculture with the oral commensal Streptococcus gordonii and the opportunistic commensal Fusobacterium nucleatum. Overall, F. nucleatum and S. gordonii perturbed the gingival epithelial cell transcriptome much less significantly than the oral pathogens Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans perturbed the transcriptome, indicating that there was a greater degree of host adaptation by the commensal species (M. Handfield, J. J. Mans, G. Zheng, M. C. Lopez, S. Mao, A. Progulske-Fox, G. Narasimhan, H. V. Baker, and R. J. Lamont, Cell. Microbiol. 7:811-823, 2005). The biological pathways significantly impacted by F. nucleatum and S. gordonii included the mitogen-activated protein kinase (MAPK) and Toll-like receptor signaling pathways. Differential regulation of GADD45 and DUSP4, key components of the MAPK pathway, was confirmed at the protein level by Western blotting. Modulation of the MAPK pathway is likely to affect host cell proliferation and differentiation. In addition, both the MAPK and Toll-like receptor pathways ultimately converge on cytokine gene expression. An enzyme-linked immunosorbent assay of secreted interleukin-6 (IL-6) and IL-8 demonstrated that F. nucleatum induced production of these cytokines, whereas S. gordonii inhibited secretion from the epithelial cells. Stimulation of secretion of proinflammatory cytokines from epithelial cells may reflect the invasive phenotype of F. nucleatum and contribute to the greater pathogenic potential of F. nucleatum than of S. gordonii.

| S-EPMC1865734 | biostudies-literature

Differential miRNA expression in gingival epithelial cells infected with Porphyromonas gingivalis

Project description:Porphyromonas gingivalis is a pathogen in severe periodontal disease. Able to exploit an intracellular lifestyle within primary gingival epithelial cells (GECs), a reservoir of P. gingivalis can persist within the gingival epithelia. This process is facilitated by manipulation of the host cell signal transduction cascades which can impact cell cycle, cell death and cytokine responses. Using microarrays, we investigated the ability of P. gingivalis 33277 to regulate microRNA (miRNA) expression in GECs. One of several miRNAs differentially regulated by GECs in the presence of P. gingivalis was miR-203, which was upregulated 4-fold compared with uninfected controls. Differential regulation of miR-203 was confirmed by qRT-PCR. Putative targets of miR-203, suppressors of cytokine signaling (SOCS) 3 and 6, were evaluated by qRT-PCR. SOCS3 and SOCS6 mRNA levels were reduced >5-fold and >2-fold, respectively, in P. gingivalis-infected GECs compared with controls. Silencing miR-203 using a si-RNA construct reversed the inhibition of SOCS3 expression. A dual luciferase assay confirmed binding of miR-203 to the putative target binding site of SOCS3 3’ UTR. Western blot analysis demonstrated that activation of Stat3, a downstream target of SOCS, was diminished following miR-203 silencing. This study shows that induction of miRNAs by P. gingivalis can modulate important host signaling responses.

2011-04-15 | GSE28635 | GEO

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

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