COMPARISON OF THE PRO-INFLAMMATORY CYTOKINE STIMULATING ACTIVITY OF THE SURFACE-ASSOCIATED PROTEINS OF PERIODONTOPATHIC BACTERIA

Saline extraction of the periodontopathic bacterium, Actinobacillus ac tinomycetemcomitans, releases surface-associated material (SAM), a com plex mixture of proteins and carbohydrates with potent biological acti ons on isolated bone and on various mammalian cell populations. In thi s study, the relative ability of the SAM from 5 organisms, implicated in the pathology of periodontal disease, to stimulate human mesenchyma l and myelomonocytic cells to synthesize the proinflammatory cytokines - interleukin (IL)-1 beta, IL-6 and tumour necrosis factor (TNF)ce ha s been investigated. The bacteria investigated were Actinobacillus act inomycetemcomitans,Eikenella corrodens, Porphyromonas gingivalis, Prev otella intermedia and Campylobacter rectus. Human cells were exposed t o a four log order range of concentrations of the SAM, or of Escherich ia coli lipopolysaccharide, to provide full agonist dose responses in order to allow comparison of the potency and efficacy of each SAM. All SAMs demonstrated the capacity to stimulate human gingival fibroblast s (HGFs), human peripheral blood mononuclear cells (PBMCs) or the myel omonocytic cell line - Mono-Mac-B to release one or all of the cytokin es assayed. Activity was heat- and trypsin-sensitive suggesting that t he active components were proteinaceous. However, there were substanti al differences in the potency and efficacy of each SAM when compared o n a concentration basis (w/v). The most active SAM was from A. actinom ycetemcomitans with those from E. corrodens and P. gingivalis being sl ightly less active. The least active cytokine-stimulating SAMs were fr om C. rectus and Pr. intermedia. One major difference between the SAMs and E. coli LPS was the inability of the former to stimulate HGFs to release IL-1 beta or TNF alpha although they could stimulate PBMCs to release these cytokines. This may have relevance to the pathology of t he periodontal diseases. (C) Munksgaard, 1996