Desulfovibrio spp. survive within KB cells and modulate inflammatory responses

C Bisson-Boutelliez,F Massin,A Lozniewski,N Miller,D Dumas

doi:10.1111/j.2041-1014.2009.00550.x

C Bisson-Boutelliez, F Massin + Show 3 more

Open Access

https://doi.org/10.1111/j.2041-1014.2009.00550.x

Copy DOI

Abstract

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.

Highlights

Periodontitis is a multifactorial disease involving complex interactions between various anaerobic bacteria and host cells, which may lead to periodontal tissue destruction
While the interaction of all these pathogens with epithelial cells may contribute to the release of inflammatory mediators, it has been shown that the expression of various cytokines, including interleukin-1b (IL-1b), IL-6, and IL-8, by epithelial cells infected with P. gingivalis may be positively correlated with its invasive capacity (Eick et al, 2006)
The invasion efficiency of these strains (0.05–0.13% of the initial inoculum) was lower than those observed with P. gingivalis ATCC 33277 (0.69% of the initial inoculum), which was used as a positive control (Houalet-Jeanne et al, 2001)

Summary

Introduction

Periodontitis is a multifactorial disease involving complex interactions between various anaerobic bacteria and host cells, which may lead to periodontal tissue destruction. Invasion potential has been shown in vitro and/ or in vivo for several bacteria associated with periodontal diseases, including Aggregatibacter actinomycetemcomitans, Eikenella corrodens, Fusobacterium nucleatum, Prevotella intermedia, Porphyromonas gingivalis, ‘Tannerella forsythia’, and Treponema denticola (Meyer et al, 1991; Duncan et al, 1993; Dorn et al, 1998; Han et al, 2000; Colombo et al, 2007). While the interaction of all these pathogens with epithelial cells may contribute to the release of inflammatory mediators, it has been shown that the expression of various cytokines, including interleukin-1b (IL-1b), IL-6, and IL-8, by epithelial cells infected with P. gingivalis may be positively correlated with its invasive capacity (Eick et al, 2006). Epithelial invasion may have a direct impact on disease progression and the inflammatory processes

Methods

Results

Discussion

Conclusion