TLR3 agonist enhances CC chemokine ligand 20 production in IL-1β-stimulated human gingival fibroblasts.

Abstract:

:Viruses are related to the etiology of periodontitis. However, the role of viruses on Th17 cells infiltration in periodontitis lesions is unknown. Therefore, we examined the effects of TLR3 ligand on CCL20, which is related to Th17 cells migration, production in human gingival fibroblasts (HGFs). Polyinosinic-polycytidylic acid (Poly I:C), which is a TLR3 agonist, stimulation could moderately induce CCL20 production in HGFs. Poly I:C synergistically enhanced CCL20 expression from IL-1β-stimulated HGFs. Inhibitors of p38 MAPK, extracellular signal-regulated kinase (ERK), c-Jun N terminal kinase (JNK), and NF-κB significantly inhibited CCL20 production in Poly I:C/IL-1β-stimulated HGFs. Western blot analysis disclosed phosphorylation of p38 MAPK, JNK, and IκB-α were enhanced in Poly I:C/IL-1β-treated HGFs. These data suggested that virus infection is related to Th17 cells migration in periodontitis lesion to induce CCL20 production in HGFs via TLR3. Therefore, our results indicated that virus might be important pathogen in periodontal disease.

journal_name

Cell Immunol

journal_title

Cellular immunology

authors

Hosokawa Y,Hosokawa I,Shindo S,Ozaki K,Matsuo T

doi

10.1016/j.cellimm.2013.05.005

subject

Has Abstract

pub_date

2013-05-01 00:00:00

pages

8-11

issue

1-2

eissn

0008-8749

issn

1090-2163

pii

S0008-8749(13)00081-6

journal_volume

283

pub_type

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