CCL20 production is induced in human dental pulp upon stimulation by Streptococcus mutans and proinflammatory cytokines.
BACKGROUND
Pulpitis is characterized by the marked infiltration of inflammatory cells in response to an invasion of caries-related bacteria. It is well known that chemokines regulate the trafficking of lymphocytes, and CC chemokine ligand 20 (CCL20) has been recently shown to play a crucial role in the recruitment of memory T cells and immature dendritic cells into inflammatory lesions. We previously reported that CCL20 was mainly expressed in microvascular endothelial cells and macrophages that accumulated in inflamed pulp tissues and that its specific receptor, CCR6, was expressed on infiltrated lymphocytes. However, the mechanism of CCL20 expression remains unclear.


RESULTS
In this study, we investigated the expression of CCL20 in monocytes/macrophages, endothelial cells, and pulpal fibroblasts after stimulation with Streptococcus mutans, a representative of caries-related bacteria, or proinflammatory cytokines. CCL20 messenger RNA was detected by reverse transcription-polymerase chain reaction in inflamed pulp, but not in clinically normal pulp. By enzyme-linked immunosorbent assay, S. mutans induced a human monocytic cell line, differentiated macrophage-like THP-1 cells, and human umbilical vein endothelial cells (HUVEC) to produce an increased amount of CCL20. Lipoteichoic acid from S. mutans also elicited CCL20 production by HUVEC. Moreover, CCL20 production from pulpal fibroblasts was increased by stimulation with inetrleukin-1beta and tumor necrosis factor-alpha.


CONCLUSIONS
Our results indicate that CCL20 expression is induced by stimulation with caries-related bacteria that have invaded deeply into the dentinal tubules as well as by proinflammatory cytokines in the inflamed pulpal lesions. It may be involved in the progression of pulpitis via accumulation of inflammatory cells.
Takahashi
K
K
Department of Conservative Dentistry, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Tokushima, Japan. tadashi@dent.tokushima-u.ac.jp
Nakanishi
T
T
Yumoto
H
H
Adachi
T
T
Matsuo
T
T
D000328:Adult; D000368:Aged; D002454:Cell Differentiation / Q000276:immunology; D002460:Cell Line; D002478:Cells, Cultured; D054418:Chemokine CCL20 / Q000235:genetics / Q000276:immunology*; D016207:Cytokines / Q000276:immunology*; D003782:Dental Pulp / Q000276:immunology* / Q000382:microbiology; D042783:Endothelial Cells / Q000276:immunology; D004730:Endothelium, Vascular / Q000276:immunology; D005260:Female; D005347:Fibroblasts / Q000276:immunology; D006801:Humans; D018836:Inflammation Mediators / Q000276:immunology*; D018799:Intercellular Adhesion Molecule-1 / Q000276:immunology; D053583:Interleukin-1beta / Q000276:immunology; D016209:Interleukin-8 / Q000276:immunology; D008070:Lipopolysaccharides / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology; D011671:Pulpitis / Q000276:immunology; D013295:Streptococcus mutans / Q000276:immunology*; D013682:Teichoic Acids / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology; D019010:Vascular Cell Adhesion Molecule-1 / Q000276:immunology
C108355:CCL20 protein, human; D054418:Chemokine CCL20; D016207:Cytokines; D018836:Inflammation Mediators; D053583:Interleukin-1beta; D016209:Interleukin-8; D008070:Lipopolysaccharides; D013682:Teichoic Acids; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; C009900:lipoteichoic acid