Odontoblasts in the dental pulp immune response

Recent studies have demonstrated that human dental pulp cells sense pathogens and elicit innate and/or adaptive immunity. Particular attention has been paid to odontoblasts that are situated at the pulp–dentin interface and constitute the first line of defense to cariogenic bacteria entering dentin...

Full description

Saved in:
Bibliographic Details
Published inJournal of experimental zoology. Part B, Molecular and developmental evolution Vol. 312B; no. 5; pp. 425 - 436
Main Authors Farges, Jean-Christophe, Keller, Jean-François, Carrouel, Florence, Durand, Stephanie H., Romeas, Annick, Bleicher, Françoise, Lebecque, Serge, Staquet, Marie-Jeanne
Format Journal Article
LanguageEnglish
Published Hoboken Wiley Subscription Services, Inc., A Wiley Company 15.07.2009
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Recent studies have demonstrated that human dental pulp cells sense pathogens and elicit innate and/or adaptive immunity. Particular attention has been paid to odontoblasts that are situated at the pulp–dentin interface and constitute the first line of defense to cariogenic bacteria entering dentin after enamel disruption. In this review, recent in vitro and in vivo data suggesting that odontoblasts initiate immune/inflammatory events within the dental pulp in response to cariogenic bacteria are discussed. These data include sensing of pathogens by Toll‐like receptors (TLRs), production of chemokines upon cell stimulation with microbial by‐products and induction of dendritic cell migration. Additional results presented here reveal that all TLR genes are expressed in the healthy human dental pulp that is thus well equipped to combat pathogens entering the tissue. Seventeen chemokine genes including CXCL12, CCL2, CXCL9, CX3CL1, CCL8, CXCL10, CCL16, CCL5, CXCL2, CCL4, CXCL11 and CCL3, and 9 chemokine receptor genes including CXCR4, CCR1, CCR5, CX3CR1, CCR10 and CXCR3, are also expressed in pulp. TLR2, CCL2 and CXCL1 are upregulated in odontoblasts both under caries lesions and upon stimulation with pathogen by‐products. These molecules thus appear as preferential targets for the design of therapeutic agents able to reduce the immune/inflammatory response to cariogenic bacteria and favor pulp healing. J. Exp. Zool. (Mol. Dev. Evol.) 312B:425–436, 2009. © 2008 Wiley‐Liss, Inc.
Bibliography:istex:8B3220390B6361B7C3D4110DF4B12D94968A3DB9
ark:/67375/WNG-563X9N22-M
ArticleID:JEZ21259
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ObjectType-Article-2
ObjectType-Feature-3
ObjectType-Review-1
ISSN:1552-5007
1552-5015
DOI:10.1002/jez.b.21259