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Prebiotic lowered candida colonization according to this study:

Dietary oligofructose and inulin protect mice from enteric and systemic pathogens and tumor inducers.
Buddington KK1, Donahoo JB, Buddington RK.
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Prebiotics induce changes in the population and metabolic characteristics of the gastrointestinal bacteria, modulate enteric and systemic immune functions, and provide laboratory rodents with resistance to carcinogens that promote colorectal cancer. There is less known about protection from other challenges. Therefore, mice of the B6C3F1 strain were fed for 6 wk a control diet with 100 g/kg cellulose or one of two experimental diets with the cellulose replaced entirely by the nondigestible oligosaccharides (NDO) oligofructose and inulin. From each diet, 25 mice were challenged by a promoter of colorectal cancer (1,2-dimethylhydrazine), B16F10 tumor cells, the enteric pathogen Candida albicans (enterically), or were infected systemically with Listeria monocytogenes or Salmonella typhimurium. The incidences of aberrant crypt foci in the distal colon after exposure to dimethylhdrazine for mice fed inulin (53%) and oligofructose (54%) were lower than in control mice (76%; P < 0.05), but the fructans did not reduce the incidence of lung tumors after injection of the B16F10 tumor cells. Mice fed the diets with fructans had 50% lower densities of C. albicans in the small intestine (P 80% for control mice), but fewer of the mice fed inulin died (60%; P < 0.05), with mice fed oligofructose again intermediate. The mechanistic basis for the increased resistance provided by dietary NDO was not elucidated, but the findings are consistent with enhanced immune functions in response to changes in the composition and metabolic characteristics of the bacteria resident in the gastrointestinal tract.

See this :

Non-digestible carbohydrates and the intestinal microflora
Compared with the cellulose and wheat fibre groups, a more than 100-fold increase in faecal lactobacilli was observed in rats fed the lactulose diet. These lactic acid bacteria were also stimulated by FOS and resistant starch, though to a lesser extent (fig 3; p<0.05). FOS and especially lactulose increased the number of bifidobacteria (fig 3; p<0.05). Lactulose, FOS, and resistant starch also increased the number of enterobacteria in faeces (fig 3; p<0.05). The levels of these bacterial genera were not affected by S enteritidis infection (data not shown).

Figure 3
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