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Influence of histamine on the expression of CCL20 in human gingival fibroblasts
Author(s) -
Dommisch H.,
Chung W. O.,
Plötz S.,
Jepsen S.
Publication year - 2015
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/jre.12265
Subject(s) - histamine , dentistry , ccl20 , periodontal fiber , chemistry , microbiology and biotechnology , biology , medicine , immunology , pharmacology , inflammation , chemokine , chemokine receptor
Background and Objective Histamine plays an important role during allergic and inflammatory reactions, and it has been suggested to influence periodontal inflammation. The aim of this study was to investigate the effects of histamine on the expression of the antimicrobial peptide C‐C chemokine ligand 20 ( CCL 20) in human gingival fibroblasts ( HGF s) when exposed to toll‐like receptor ( TLR ) agonists. Material and Methods Monolayers of HGF s from three different donors were exposed to histamine, alone, and in combination with Pam3 CSK 4 (a TLR 2 agonist) or lipopolysaccharide ( LPS ) from Escherichia coli (a TLR 4 agonist), for 2, 4, 6 or 12 h. In another experimental group, cells were pretreated with a specific histamine‐1 receptor antagonist (H1R) antagonist, cetirizine. Real‐time PCR analysis was performed to detect expression of glyceraldehyde‐3‐phosphate dehydrogenase ( GAPDH ), CCL 20 and interleukin‐8 ( IL 8 ) genes. The levels of CCL 20 and IL ‐8 protein were determined by ELISA . Results In HGF s, histamine induced expression of CCL 20 and IL 8 genes in a time‐dependent manner ( p < 0.05). Combined stimulation with histamine and Pam3 CSK 4 or LPS led to a significant amplification in expression of CCL 20 and IL ‐8 when compared with treatment with each stimulant alone ( p < 0.05), and this effect was mediated via pathways involving the H1R ( p < 0.05). Conclusion The results of this study suggest a sensitizing effect of histamine on early innate immune responses of HGF s when simultaneously exposed to bacterial virulence factors.