Premium
Effects and interactions of tumour necrosis factor α and bradykinin on interleukin‐1 production in gingival fibroblasts
Author(s) -
YucelLindberg T.,
Lerner U.H.,
Modéer T.
Publication year - 1995
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/j.1600-0765.1995.tb01272.x
Subject(s) - protein kinase c , bradykinin , tumor necrosis factor alpha , cytokine , phorbol , endocrinology , chemistry , beta (programming language) , interleukin , medicine , tetradecanoylphorbol acetate , microbiology and biotechnology , biology , kinase , biochemistry , receptor , computer science , programming language
Summary Effects of and interactions between tumour necrosis factor α (TNFα) and bradykinin (BK) on production of interleukin‐1 (IL‐lα, IL‐lβ) in human gingival fibroblasts were studied. The cytokine TNFα induced production of cell‐associated IL‐lα and IL‐1β in gingival fibroblasts, with IL‐lβ being most abundant. Addition of BK, in the presence of TNFα, for 1 h and 6 h, respectively, synergistically enhanced the TNFα induced IL‐lβ production, whereas BK alone did not induce 1L‐1 production. Similar to BK, two phorbol esters, phorbol 12,13 dibutyrate (PDBu) and phorbol 12‐myristate‐13‐acetate (PMA) which are known to stimulate protein kinase C (PKC), synergistically enhanced the TNFα induced IL‐lβ production in the gingival fibroblasts. On the contrary, a phorbol ester which does not activate protein kinase C, 13‐phorbolacetate (13‐PA), did not potentiate the TNFα induced IL‐lβ production. Similar to BK, the phorbol esters (PMA, PDBu, 13‐PA) alone did not induce IL‐1β production in the gingival fibroblasts. The results indicate that TNFα induces production of cell‐associated IL‐1 in gingival fibroblasts, which can be upregulated by a PKC dependent pathway.