Microbial inhibition of oral epithelial wound recovery: potential role for quorum sensing molecules?

Abstract

Awareness of the impact of microbiota in both health and disease is growing. Using a new in vitro oral mucosa co-culture model, we recently showed a clear inhibition of epithelial wound healing in the presence of an oral microbial community. In this paper, we have used the same model in combination with specific oral microbial species to obtain a better insight into the role of the oral microbiota in wound healing. Monocultures of Klebsiellaoxytoca and Lactobacillus salivarius significantly inhibited wound healing with ~20%, whereas Streptococcus mitis and S. oralis enhanced the healing process with ~15% in 24 h. Yet, neither S. oralis or S. mitis were able to counteract the inhibitory effects from K.oxytoca on wound healing. Other tested microbial species had no effect on wound healing. Apart from this species-dependency, the inhibitory effect on wound healing depended on a microbial threshold concentration. Further mechanistic experiments with K.oxytoca excluded different microbial factors and hypothesized that quorum sensing molecules might play a role in the inter-kingdom signalling during wound healing. These results are important for the development of new strategies for the management of (infected) wounds and ulcerations.Electronic supplementary materialThe online version of this article (doi:10.1186/s13568-015-0116-5) contains supplementary material, which is available to authorized users.

Lactobacillus crispatus accelerates re‐epithelialization in vaginal epithelial cell line MS74

“…28,[38][39][40] On the other hand, L. salivarius and L. plantarum inhibited oral epithelial wound healing. 41 A recent study showed that a bioengineered L. reuteri with a plasmid encoding CXCL12 accelerated cutaneous wound healing in mouse, while nontransformed L. reuteri delayed wound closure. 42 In the present study, we demonstrated that 43 L. crispatus and its supernatant decreased proinflammatory cytokines and increased IL-10 production by HeLa cells in the presence of Chlamydia trachomatis.…”

Streptococcus salivarius MS-oral-D6 promotes gingival re-epithelialization in vitro through a secreted serine protease

“…The desalted samples were divided in two equal volume aliquots, one of which was treated with 200 μg/ml proteinase K (1 hour at 37 °C) and the other was left untreated. Inactivation of proteinase K was accomplished by heating the samples to 98 °C for 10 minutes, followed by centrifugation (16,000 × g, 10 min at room temperature) 62 . After centrifugation, all samples were filtered sterilized (0.2 μm, Whatman, GE Healthcare Life Sciences) and then stored at −80 °C until used.…”

Tilivalline- and Tilimycin-Independent Effects of Klebsiella oxytoca on Tight Junction-Mediated Intestinal Barrier Impairment

“…In a study on oral epithelial wound recovery, De Ryck and colleagues already pointed out that K. oxytoca must secret other effector molecules beyond tilivalline and tilimycin. They hypothesized that K. oxytoca -produced quorum-sensing molecules might contribute to its inhibitory impact on wound healing [24]. Former studies showed the toxicity of culture supernatant of K. oxytoca derived from patients with AAHC was not inactivated by 60 °C treatment, but was sensitive to 100 °C [25].…”