RESUMEN
Oral probiotics are increasingly used in the harmonization of the oral microbiota in the prevention or therapy of various oral diseases. Investigation of the antimicrobial activity of the bacteriocinogenic strain Streptococcus salivarius K12 against oral pathogens shows promising results, not only in suppressing growth, but also in eliminating biofilm formation. Based on these findings, we decided to investigate the antimicrobial and antibiofilm activity of the neutralized cell-free supernatant (nCFS) of S. salivarius K12 at various concentrations against selected potential oral pathogens under in vitro conditions on polystyrene microtiter plates. The nCFS of S. salivarius K12 significantly reduced growth (p < 0.01) in Streptococcus mutans Clarke with increasing concentration from 15 to 60 mg/mL and also in Staphylococcus hominis 41/6 at a concentration of 60 mg/mL (p < 0.001). Biofilm formation significantly decreased (p < 0.001) in Schaalia odontolytica P10 at nCFS concentrations of 60 and 30 mg/mL. Biofilm inhibition (p < 0.001) was also observed in Enterobacter cloacae 4/2 at a concentration of 60 mg/mL. In Schaalia odontolytica P10 and Enterobacter cloacae 4/2, the nCFS had no effect on their growth.
RESUMEN
The aim of this study was to investigate the use of a standardized animal model subjected to antibiotic treatment, and the effects of this treatment on the course of dextran sodium sulphate (DSS)-induced colitis in mice. By decontamination with selective antibiotics and observation of pathogenesis of ulcerative colitis (UC) induced chemically by exposure of mice to various concentrations of DSS, we obtained an optimum animal PGF model of acute UC manifested by mucin depletion, epithelial degeneration and necrosis, leading to the disappearance of epithelial cells, infiltration of lamina propria and submucosa with neutrophils, cryptitis, and accompanied by decreased viability of intestinal microbiota, loss of body weight, dehydration, moderate rectal bleeding, and a decrease in the selected markers of cellular proliferation and apoptosis. The obtained PGF model did not exhibit changes that could contribute to inflammation by means of alteration of the metabolic status and the induced dysbiosis did not serve as a bearer of pathogenic microorganisms participating in development of ulcerative colitis. The inflammatory process was induced particularly by exposure to DSS and its toxic action on compactness and integrity of mucosal barrier in the large intestine. This offers new possibilities of the use of this animal model in studies with or without participation of pathogenic microbiota in IBD pathogenesis.