Literature DB >> 15111638

Induction of tolerance by Porphyromonas gingivalis on APCS: a mechanism implicated in periodontal infection.

N Cohen1, J Morisset, D Emilie.   

Abstract

The periodontal pathogen Porphyromonas gingivalis (Pg) is a potent inducer of the production of pro-inflammatory cytokines by neutrophils, monocytes, and macrophages, and can desensitize immune cells in vitro and in vivo. We analyzed the ability of Pg lipopolysaccharide (LPS) to induce endotoxin tolerance. Treatment of dendritic cells (DC), the human macrophage cell line THP-1, and monocytes (antigen-presenting cells, APC) with Pg.LPS inhibited APC maturation assessed by CD80 and CD86 expression, and inhibited chemokine (CCL3 and CCL5) production. Pre-treatment with glucocorticoids (GC) and interleukin-10 (IL-10) abolished the effect of Pg.LPS on CD80, CD83, and CD86, and on CCL3 and CCL5 production. We also showed that Pg.LPS enhanced the tolerogenic properties of APCs and up-regulated ILT-3 and B7-H1 expression.

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Year:  2004        PMID: 15111638     DOI: 10.1177/154405910408300515

Source DB:  PubMed          Journal:  J Dent Res        ISSN: 0022-0345            Impact factor:   6.116


  16 in total

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Review 2.  Dendritic cells at the oral mucosal interface.

Authors:  C W Cutler; R Jotwani
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Authors:  Jeffrey L Ebersole; Dolphus R Dawson; Lorri A Morford; Rebecca Peyyala; Craig S Miller; Octavio A Gonzaléz
Journal:  Periodontol 2000       Date:  2013-06       Impact factor: 7.589

6.  Differential Gene Expression Profiles Reflecting Macrophage Polarization in Aging and Periodontitis Gingival Tissues.

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7.  Oral mucosal endotoxin tolerance induction in chronic periodontitis.

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9.  Immunologic environment influences macrophage response to Porphyromonas gingivalis.

Authors:  G Papadopoulos; Y B Shaik-Dasthagirisaheb; N Huang; G A Viglianti; A J Henderson; A Kantarci; F C Gibson
Journal:  Mol Oral Microbiol       Date:  2016-08-26       Impact factor: 3.563

10.  The inhibitory receptor LILRB4 (ILT3) modulates antigen presenting cell phenotype and, along with LILRB2 (ILT4), is upregulated in response to Salmonella infection.

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