This study demonstrated the capacity of bacteriocin-producing lactic acid bacteria (LAB) to reduce intestinal colonization by vancomycin-resistant enterococci (VRE) in a mouse model. Lactococcus lactis MM19 and Pediococcus acidilactici MM33 are bacteriocin producers isolated from human feces. The bacteriocin secreted by P. acidilactici is identical to pediocin PA-1/AcH, while PCR analysis demonstrated that L. lactis harbors the nisin Z gene. LAB were acid and bile tolerant when assayed under simulated gastrointestinal conditions. A well diffusion assay using supernatants from LAB demonstrated strong activity against a clinical isolate of VRE. A first in vivo study was done using C57BL/6 mice that received daily intragastric doses of L. lactis MM19, P. acidilactici MM33, P. acidilactici MM33A (a pediocin mutant that had lost its ability to produce pediocin), or phosphate-buffered saline (PBS) for 18 days. This study showed that L. lactis and P. acidilactici MM33A increased the concentrations of total LAB and anaerobes while P. acidilactici MM33 decreased the Enterobacteriaceae populations. A second in vivo study was done using VRE-colonized mice that received the same inocula as those in the previous study for 16 days. In L. lactis-fed mice, fecal VRE levels 1.73 and 2.50 log 10 CFU/g lower than those in the PBS group were observed at 1 and 3 days postinfection. In the P. acidilactici MM33-fed mice, no reduction was observed at 1 day postinfection but a reduction of 1.85 log 10 CFU/g was measured at 3 days postinfection. Levels of VRE in both groups of mice treated with bacteriocin-producing LAB were undetectable at 6 days postinfection. No significant difference in mice fed the pediocin-negative strain compared to the control group was observed. This is the first demonstration that human L. lactis and P. acidilactici nisin-and pediocin-producing strains can reduce VRE intestinal colonization.

To assess the potential of Lactobacillus acidophilus and Lactobacillus casei strains to increase the apoptosis of a colorectal cancer cell line in the presence of 5-fluorouracil (5-FU), LS513 colorectal cancer cells were treated for 48 h with increasing concentrations of these lactic acid bacteria (LAB) in the presence of 100 mu g/ml of 5-FU. In the presence of 10(8) CFU/ml of live LAB, the apoptotic efficacy of the 5-FU increased by 40%, and the phenomenon was dose dependent. Moreover, irradiation-inactivated LAB caused the same level of induction, whereas microwave-inactivated LAB reduced the apoptotic capacity of the 5-FU. When cells were treated with a combination of live LAB and 5-FU, a faster activation of caspase-3 protein was observed, and the p21 protein seems to be downregulated. These results suggest that live L. acidophilus and L. casei are able to increase the apoptosis-induction capacity of 5-FU. The mechanisms of action are still not elucidated, and more research is needed to understand them. This is the first set of experiments demonstrating that some strains of LAB can enhance the apoptosis-induction capacity of the 5-FU. Based on these results, it is possible to speculate that LAB or probiotics could be used as an adjuvant treatment during anticancer chemotherapy.

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