INTERACTIONS BETWEEN PERIODONTOPATHOGENIC BACTERIA AND CYTOKINES

Citation
J. Fletcher et al., INTERACTIONS BETWEEN PERIODONTOPATHOGENIC BACTERIA AND CYTOKINES, Journal of Periodontal Research, 32(1), 1997, pp. 200-205
Citations number
11
Categorie Soggetti
Dentistry,Oral Surgery & Medicine
ISSN journal
00223484
Volume
32
Issue
1
Year of publication
1997
Part
2
Pages
200 - 205
Database
ISI
SICI code
0022-3484(1997)32:1<200:IBPBAC>2.0.ZU;2-B
Abstract
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.