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IL ‐17 stimulates the production of the inflammatory chemokines IL ‐6 and IL ‐8 in human dental pulp fibroblasts
Author(s) -
Xiong H.,
Wei L.,
Peng B.
Publication year - 2015
Publication title -
international endodontic journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.988
H-Index - 119
eISSN - 1365-2591
pISSN - 0143-2885
DOI - 10.1111/iej.12339
Subject(s) - chemokine , pulpitis , pulp (tooth) , kinase , p38 mitogen activated protein kinases , interleukin 33 , microbiology and biotechnology , signal transduction , chemistry , mapk/erk pathway , interleukin , cytokine , inflammation , biology , immunology , medicine , pathology
Aim To investigate IL‐17 expression in human pulpitis and to study the effects of IL‐17 on the secretion of the chemokines IL‐6 and IL‐8 and the related signalling pathways. Methodology Samples of human dental pulp tissue were obtained from healthy controls and patients with pulpitis. Cytokine IL‐17 messenger RNA (mRNA) expression in the pulp tissue was detected by real‐time polymerase chain reaction. In addition, human dental pulp fibroblasts (HDPFs) were stimulated with IL‐17. Production of IL‐6 and IL‐8 was determined by reverse transcriptase‐polymerase chain reaction and enzyme‐linked immunosorbent assay. Aspects of the nuclear factor‐kappa B (NF‐κB) and mitogen‐activated protein kinases (MAPKs) signalling pathways were examined by Western blot analysis. Result Increased levels of IL‐17 mRNA were found in inflamed dental pulp tissue (pulpitis). Stimulation of dental pulp tissue with IL‐17 induced the production of IL‐6 and IL‐8 in a dose‐dependent manner. In addition, IL‐17 stimulation resulted in rapid activation of nuclear factor‐kappaB (NF‐κB), phosphorylation of p38 MAPK, extracellular signal‐regulated kinase (ERK) and Jun N‐terminal kinase (JNK) in HDPFs. Conclusion IL‐17 may participate in pulp tissue inflammation through chemokine production and NF‐κB and MAPKs signalling pathways.