Influence of Monolaurin on Metabolome Using a Bacteria/Cell Co-culture Model

Objectives: The periodontal disease is characterized by chronic oral bacterial infection associated with the presence of biofilm. Monolaurin presents antibacterial and antiviral activity in vitro, which may be of great interest in the treatment and/or prevention of various infections. However its effect on periodontopathogenic bacteria has yet to be determined.
The aim of this in vitro study were to evaluate the monolaurin effects on the metabolome using a bacteria/cell co-culture model inoculated with Aggregatibacter actinomycetemcomitans (Aa).
Methods: The antimicrobial activity of the Monolaurin (1-lauroyl-rac-glycerol) was tested in Aa and your citotoxicity effects were tested in oral fibroblast and keratinocites. Fibroblasts (1x10⁵) were seeded into a 24 well plate (basal chamber). Transwell inserts (apical chamber) were positioned into the 24 well plate and keratinocites (1x10⁵) were seeded. After 24 hours, the media of the basal and apical chamber were replaced with new media and Aa (1x10⁶cfu/mL) were inoculated on apical chamber. Immediately after the inoculation with Aa the Monolaurin treatments (25µM and 50µM) were added and the plate was incubated at 37^oC in humid air containing 5% CO₂. The time of exposure of the microorganism to Monolaurin was 24 hours. Each experiment was repeated three times with two replicates per group (n=6). After treatment period, the supernatant were collected for metabolome analysis.
Results: The metabolome study returned a total of 282 metabolites. Some metabolites presented significantly-altered concentrations. The monolaurin treatment (25µM and 50µM) increased (P<0.05) the concentrations of pyruvic acid and glycerol, when compared to untreated control. On the other hand, the concentrations of pinitol, 4-aminobutyric acid and glyceric acid were reduced (P<0.05) due to the treatment with 25 µM of monolaurin.
Conclusions: The Monolaurin was able to affect the concentration of pinitol, 4-aminobutyric acid and glyceric acid and these changing may indicate an improvement in the host response to infection by Aa.
Supported by NIH/NCCAM (R00AT00650704) and CAPES