Yamazaki K, Polak B, Bird P S, Gemmell E, Hara K, Seymour G J
Oral Microbiol Immunol. 1989 Dec;4(4):193-8. doi: 10.1111/j.1399-302x.1989.tb00251.x.
The effect of heat-killed periodontopathic bacteria on the production of interleukin-1 (IL-1) and an IL-1 inhibitor by human polymorphonuclear neutrophils (PMN's) was examined. Peripheral blood was obtained from 18 healthy volunteers and the PMN's were separated using dextran sedimentation and Ficoll-Paque density gradient centrifugation. The PMN's (5 x 10(5) cells/well) were cultured in serum-free media with or without heat-killed periodontopathic bacteria. Four gram-negative periodontopathic bacteria were used; Bacteroides gingivalis FDC 381, Bacteroides forsythus FDC 338, Actinobacillus actinomycetemcomitans Y4 and Fusobacterium nucleatum FDC 263. The non-oral Fusobacterium mortiferum ATCC 25557 was used as a control organism. IL-1 activity was assayed using thymocyte proliferation. The non-oral organism F. mortiferum stimulated IL-1 production by PMN's, in contrast none of the periodontopathic bacteria stimulated IL-1 release although the bacteria themselves had an IL-1 enhancing effect. Following fractionation of the periodontopathic bacteria stimulated PMN supernatants, an IL-1 inhibitory fraction was identified. These results may illustrate a further mechanism by which periodontopathic bacteria may evade the protective effect of PMN's and may also suggest a regulatory role for PMN's in chronic inflammatory periodontal disease.