Effects and interactions of tumour necrosis factor alpha and bradykinin on interleukin-1 production in gingival fibroblasts.
J Periodontal Res
; 30(3): 186-91, 1995 May.
Article
em En
| MEDLINE
| ID: mdl-7473001
ABSTRACT
Effects of and interactions between tumour necrosis factor alpha (TNF alpha) and bradykinin (BK) on production of interleukin-1 (IL-1 alpha, IL-1 beta) in human gingival fibroblasts were studied. The cytokine TNF alpha induced production of cell-associated IL-1 alpha and IL-1 beta in gingival fibroblasts, with IL-1 beta being most abundant. Addition of BK, in the presence of TNF alpha, for 1 h and 6 h, respectively, synergistically enhanced the TNF alpha induced IL-1 beta production, whereas BK alone did not induce IL-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 TNF alpha induced IL-1 beta 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 TNF alpha induced IL-1 beta production. Similar to BK, the phorbol esters (PMA, PDBu, 13-PA) alone did not induce IL-1 beta production in the gingival fibroblasts. The results indicate that TNF alpha induces production of cell-associated IL-1 in gingival fibroblasts, which can be upregulated by a PKC dependent pathway.
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Base de dados:
MEDLINE
Assunto principal:
Bradicinina
/
Interleucina-1
/
Fator de Necrose Tumoral alfa
/
Fibroblastos
/
Gengiva
Limite:
Child
/
Humans
Idioma:
En
Ano de publicação:
1995
Tipo de documento:
Article