Effects of Bdellovibrio bacteriovorus HD100 on experimental periodontitis in rats

Abstract

Aim The aim of this study was to evaluate the effects of Bdellovibrio bacteriovorus HD100 on experimental periodontitis (EP) in rats. Methods Thirty‐two rats were divided into four groups: control, C‐HD100 (B. bacteriovorus), EP, and EP‐HD100. On day 0, EP was induced by the placement of cotton ligatures around the mandibular first molars (MFMs) in the EP and EP‐HD100 groups. In the C‐HD100 and EP‐HD100 groups, suspensions containing 1 × 109 PUF/ml of B. bacteriovorus HD100 were topically administered to the subgingival region of MFMs on days 0, 3, and 7. Animals were euthanized on day 14. Morphometrics analyses were performed in hemimandibles. The levels of tumor necrosis factor alpha (TNF‐α), interleukin (IL)‐6, monocyte chemoattractant protein (MCP)‐1, IL‐10, IL‐1β, transforming growth factor beta (TGF‐β), macrophage colony‐stimulating factor (M‐CSF) and regulated on activation and normal T cell expressed and secreted (RANTES) were determined by enzymatic immunoassays in gingival tissues. Beta defensin (BD)‐1, BD‐2, and BD‐3, Toll‐like receptors (TLR)‐2 and TLR‐4, and a cluster of differentiation (CD)‐4, CD‐8 and CD‐57 were analyzed by immunohistochemistry in hemimandibles. Data were statistically analyzed. Results The EP group showed greater alveolar bone loss than EP‐HD100 (p < .05). The EP‐HD100 group showed higher levels of MCP‐1, RANTES, IL‐10, and TGF‐β, lower levels of TNF‐α than the EP group (p < .05). No differences were observed in IL‐1β, IL‐6, and M‐CSF levels between EP and EP‐HD100 groups. The C‐HD100 group had higher IL‐6, TNF‐α, RANTES, and MCP‐1 levels than the control group (p < .05). Regarding BD, the EP‐HD100 group showed a larger immunolabeling pattern for BD‐1, BD‐2, and BD‐3 than the EP group (p < .05). No significant differences in the immunolabeling pattern were observed for TLR‐2, TLR‐4, CD‐4, CD‐8, and CD‐57 between EP and EP‐HD100 groups. Conclusion The topical use of B. bacteriovorus HD100 reduces alveolar bone loss, increases expression of BD, and modulates the cytokines levels on periodontal tissues in rats with EP.

Predatory bacteria prevent the proliferation of intraocular Serratia marcescens and fluoroquinolone-resistant Pseudomonas aeruginosa

“…It has been demonstrated that Bdellovibrio bacteriovorus are indifferent to the antibiotic-resistance status of their prey [6,7]. Moreover, it has been demonstrated that predatory bacteria are nontoxic to mammalian cells and in animal models and have the ability to attenuate Gram-negative bacteria in several in vivo models, including but not limited to airway and oral infections in rodents and central nervous system infection of zebrafish hindbrain ventricles [8][9][10][11][12][13][14][15][16].…”

Intra-ocular Predation of Fluoroquinolone-ResistantPseudomonas aeruginosaandSerratia marcescensby Predatory Bacteria

“…It has been demonstrated that predatory bacteria are indifferent to the antibiotic-resistance status of their prey [6,7]. Moreover, it has been demonstrated that predatory bacteria are non-toxic to mammalian cells and in animal models and have the ability to attenuate Gram-negative bacteria several in vivo models, including but not limited to airway and oral infections in rodents and central nervous system infection of zebrafish hindbrain ventricles [8][9][10][11][12][13][14][15][16].…”