Effects of intestinal microflora on the development of colonic neoplasm induced by 1,2-dimethylhydrazine (DMH) were observed using conventionalized and gnotobiotic mouse models. The incidence of colonic adenoma in germ-free mice (IQI/jic) (GF), mice conventionalized after DMH injection (Cvz-post-DMH) and conventionalized mice (Cvz, conventionalized before DMH injection) was 74%, 69% and 58%, respectively. The mean number of adenomas per mouse in the three groups was 2.6, 2.0 and 1.4, respectively. However, the adenoma in Cvz was larger than in GF. The incidence of adenoma in mice mono-associated with Mitsuokella multiacida, Clostridium butyricum, Bifidobacterium longum, Clostridium paraputrificum, Escherichia coli and Lactobacillus acidophilus was 68%, 68%, 63%, 50%, 50% and 30%, respectively. However, the adenoma in the Cl. paraputrificum group and the Cl. butyricum group was larger than in GF. Faecal pH in Cvz and the L. acidophilus group was significantly lower than in GF. The deconjugation rate of faecal bile acids in Cvz, the Cl. paraputrificum group and the Cl. butyricum group was significantly higher than in GF. These findings suggested two different effects of microflora on the development of DMH-induced adenoma: either an inhibition of the incidence of adenoma or a promotion of tumour growth. Effects of L. acidophilus may be mediated by faecal pH and effects of Cl. paraputrificum and Cl. butyricum by deconjugated bile acids.
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