Desulfovibrio spp. survive within KB cells and modulate inflammatory responses.

Desulfovibrio are sulfate-reducing anaerobic gram-negative rods that have been proposed as potential periodontopathogens. We investigated the capacity of Desulfovibrio to invade epithelial cells and induce cytokine secretion from these cells. Desulfovibrio strains were co-cultured with KB cells and counts of intracellular bacteria evaluated up to 3 days after infection. Desulfovibrio desulfuricans and Desulfovibrio fairfieldensis were able to survive within epithelial cells. Intracytoplasmic location of both bacterial species was confirmed by confocal laser scanning microscopy and transmission electron microscopy. Invasion was sensitive to nocodazole, an inhibitor of microtubule polymerization, but not to cytochalasin D, a microfilament inhibitor, suggesting that microtubule rearrangements were involved in the internalization of Desulfovibrio strains by KB cells. Infection by Desulfovibrio resulted in increased production of IL-6 and IL-8 by KB cells. The ability of D. desulfuricans and D. fairfieldensis to survive within oral epithelial cells and to modulate the epithelial immune response may contribute to the initiation and progression of periodontal diseases.

Isolation of the provisionally named Desulfovibrio fairfieldensis from human periodontal pockets.

Sulfate-reducing bacteria have recently been associated with periodontitis and proposed to play a role in the pathogenesis of this chronic inflammatory process. Eight isolates of sulfate-reducing bacteria belonging to the genus Desulfovibrio were obtained from the periodontal pockets of five out of seven patients presenting with active periodontitis. A multiplex PCR was devised for their identification at the species level. All isolates were identified as Desulfovibrio fairfieldensis, a recently proposed new species. This finding reinforces the suggestion that Desulfovibrio fairfieldensis is a human bacterium that may present a pathogenic potential.

CD9 and HLA-DR expression by crevicular epithelial cells and polymorphonuclear neutrophils in periodontal disease.

BACKGROUND, AIMS: The composition of gingival crevicular fluid (GCF) is likely to reflect inflammatory modifications that take place in the gingiva during periodontal diseases. METHOD: In this study, GCF was collected at 3 different sites from 23 periodontal patients. The sites were assessed to be healthy, presenting gingivitis or periodontitis. 10 healthy individuals without any form of periodontal disease formed the control group and were sampled at one site each. The cell content of GCF was collected using Durapore Millipore strips, and 2 types of cells were studied: epithelial cells (EC) and polymorphonuclear neutrophils (PMN). The expression of CD9 and HLA-DR within or on the surface of these cells was studied in immunofluorescence on cytospin smears. RESULTS: Both CD9 and HLA-DR expression on EC differed significantly from control subjects, and the latter decreased according to the severity of the pathology. None of the PMN found in controls expressed CD9 or HLA-DR. However, in periodontal patients, the expression of HLA-DR within PMNs was detectable and increased according to the severity of lesions. CD9 expression on PMNs also increased with inflammation. CONCLUSION: This study shows that clinically healthy sites of periodontal patients already present signs of immunological activation characterised by a down modulation of HLA-DR expression on EC and an upregulation of these 2 molecules in PMN.