Cytokines produced in response to plaque bacteria clearly play a key r
ole in the periodontal diseases. However, we know very little about th
e interactions between cytokines and periodontopathogenic bacteria. Th
e aims of this study were to determine whether the key pro-inflammator
y cytokines interleukin-1 beta (IL-1 beta) and IL-6 could affect the g
rowth of Actinobacillus actinomycetemcomitans or Porphyromonas gingiva
lis and to determine whether these organisms could hydrolyse IL-1 beta
, IL-6 or the anti-inflammatory IL-1 receptor antagonist (IL-1ra). Cul
ture medium containing up to 100 ng/ml of IL-1 beta or IL-6 was inocul
ated with A. actinomycetemcomitans (serotypes a, b and c) or P. gingiv
alis and growth was monitored by measuring changes in electrical condu
ctivity every 3 min for up to 48 h. IL-1 beta, IL-6 or IL-1ra were add
ed to culture supernatants and incubated for up to 24 h. Samples were
taken at various times, analysed by SDS-PAGE and the separated protein
s transferred by Western blotting to PVDF membranes and probed with an
ticytokine antibodies. None of the cytokines tested had any effect on
the rate of growth or yield of A. actinomycetemcomitans or P. gingival
is. Supernatants front P. gingivalis cultures, but not those from A. a
ctinomycetemcomitans, hydrolysed IL-1 beta, IL-6 and IL-1ra. The hydro
lysate from the P. gingivalis supernatant-treated IL-1 beta was unable
to stimulate the release of IL-6 from human gingival fibroblasts show
ing that it had lost biological activity. These results suggest that P
. gingivalis can perturb the cytokine network, not only by stimulating
the release of cytokines from host cells, but also by removing them f
rom its local environment.