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. 2006 Sep;72(9):5799-805.
doi: 10.1128/AEM.00109-06.

Selecting lactic acid bacteria for their safety and functionality by use of a mouse colitis model

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Selecting lactic acid bacteria for their safety and functionality by use of a mouse colitis model

Catherine Daniel et al. Appl Environ Microbiol. 2006 Sep.

Abstract

Studies showed that specific probiotics might provide therapeutic benefits in inflammatory bowel disease. However, a rigorous screening of new probiotics is needed to study possible adverse interactions with the host, particularly when intended for administration to individuals with certain health risks. In this context, the objective of this study was to investigate the role of three lactobacilli (LAB) on intestinal inflammation and bacterial translocation using variations of the mouse model of 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced acute colitis. We first compared the in vitro ability of LAB to survive gastrointestinal tract (GIT) conditions and their ability to persist in the GIT of mice following daily oral administration. As a control, we included a nonprobiotic Lactobacillus paracasei strain, previously isolated from an endocarditis patient. Feeding high doses of LAB strains to healthy and to TNBS-treated mice did not induce any detrimental effect or abnormal translocation of the bacteria. Oral administration of Lactobacillus salivarius Ls-33 had a significant preventive effect on colitis in mice, while Lactobacillus plantarum Lp-115 and Lactobacillus acidophilus NCFM did not. None of the three selected LAB strains translocated to extraintestinal organs of TNBS-treated mice. In contrast, L. paracasei exacerbated colitis under severe inflammatory conditions and translocated to extraintestinal organs. This study showed that evaluations of the safety and functionality of new probiotics are recommended. We conclude that not all lactobacilli have similar effects on intestinal inflammation and that selected probiotics such as L. salivarius Ls-33 may be considered in the prevention or treatment of intestinal inflammation.

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Figures

FIG. 1.
FIG. 1.
Fecal counts of L. plantarum NCIMB8826(pNZYR), L. plantarum Lp-115(pNZYR), L. salivarius Ls-33(pNZYR), L. paracasei subsp. paracasei YS8866441, and L. acidophilus NCFM(pNZYR) administered intragastrically for four consecutive days (days 1 to 4) in mice (n = 5). Data are the arithmetic means of results from three separate experiments (CFU/100 mg feces).
FIG. 2.
FIG. 2.
Effects of IG administration of L. salivarius Ls-33(pNZYR), L. plantarum Lp-115(pNZYR), L. acidophilus NCFM(pNZYR), and L. paracasei YS8866441 on macroscopic damage induced by two distinct doses of TNBS: (A) 120 mg/kg and (B) 150 mg/kg body weight. Results are expressed as mean Wallace scores of the group (n = 10) ± SEM (significantly different from the corresponding TNBS-control group [*, P < 0.05; **, P < 0.01]). Body weight variation is expressed as mean values of the percentage of weight loss of each group ± SEM between day 7 (sacrifice) and day 5 (TNBS). Mortality corresponds to numbers of individual dead mice (+).
FIG. 3.
FIG. 3.
Bacterial translocation in liver, spleen, kidney, and MLNs of TNBS-treated mice (150 mg/kg; very strong colitis) IG administered Ls-33(pNZYR), NCFM(pNZYR), Lp-115(pNZYR), YS8866441, or carbonate buffer (TNBS+ control) (n = 10 mice/group). Carbonate buffer was administered to a negative control group of healthy mice (ctrl−) (significantly different from the corresponding TNBS-positive control group [*, P < 0.05; **, P < 0.01]). (A) Translocation of specific administered LAB strains (enumerated on MRS agar plus the respective antibiotic). (B) Translocation of gram-positive bacteria from total endogenous flora (enumerated on MRS agar). Results presented (numbers of CFU/g of individual organ) are the arithmetic means ± standard errors of the means.

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