Evidence indicates that consumption of probiotic microorganisms such as bifidobacteria reduces the risk of colon cancer in animal models. Feeding certain fructans such as oligofructose and inulin, which are thought to selectively increase the growth of intestinal bifidobacteria (i.e., a prebiotic effect), also has been shown to reduce colon cancer risk. The objective of our study was twofold, i. e., to determine whether the combination of bifidobacteria and oligofructose would have an additive effect (i.e., synbiotic) in reducing colon cancer risk in rats, and to determine whether other oligosaccharides would also be effective as part of a synbiotic combination. The development of colonic preneoplastic lesions (aberrant crypts) was used as an index of colon cancer risk. In one series of experiments, rats were given the carcinogen 1, 2-dimethylhydrazine (DMH) and administered one of the following treatments: skim milk (control), bifidobacteria (bifido), oligofructose (OF) or bifido + OF. Neither bifido nor OF alone significantly reduced aberrant crypt number. Bifido + OF reduced aberrant crypt number in five of six experiments, although the reduction was significant in only one. However, a paired comparison of the six experiments indicated a significant overall reduction in aberrant crypts by bifido + OF (P = 0.039). Soybean oligosaccharide (SBO) and wheat bran oligosaccharide (WBO) were also fed in combination with bifidobacteria. In two other experiments, SBO did not alter the number of aberrant crypts compared with the control, whereas WBO reduced aberrant crypt number in one experiment but not in another. Of OF, SBO and WBO, only SBO reduced the colonic mucosa proliferation compared with the control. These results suggest that the combination of bifidobacteria and oligofructose reduces colon cancer risk in carcinogen-treated rats, but the effect of other oligosaccharides is uncertain.
Interactions between host plasminogen (Plg) and streptokinase (SK) secreted by group A streptococci (GAS) have been hypothesized to promote bacterial invasion of tissues. The virulence of GAS strain UMAA2616, after being subcutaneously inoculated into mice, was studied. Skin lesions and mortality were observed after inoculation of 7x106 cfu. Coadministration of human Plg with UMAA2616 markedly increased virulence. SK-deficient UMAA2616 (UMAA2616-SK(-)) was generated. Mean skin-lesion area and mortality, after bacterial inoculation (3x105 cfu), were significantly greater with UMAA2616 in the presence of human Plg than with UMAA2616-SK(-) in the presence of human Plg (P=.0001). Human Plg also enhanced UMAA2616-SK(-) virulence. Exogenous human Plg enhanced the virulence of MGAS166, a human clinical isolate. These findings suggest that SK-Plg interactions are an important determinant of GAS invasiveness in vivo and that both SK and host Plg activators appear to promote virulence of GAS by catalyzing plasmin formation.
Although epidemiological studies have implicated red meat as increasing colon cancer risk, animal studies have generally not been supportive of such an effect. This study examined red meat components, such as beef protein and tallow, on markers of colon cancer risk. Rats administered dimethylhydrazine were fed either casein or beef protein as the protein source and soybean oil or tallow as the fat source in a 2 2 factorial design for 9 wk. There were fewer preneoplastic lesions [aberrant crypt foci (ACF)] and a greater apoptotic labeling index (P < 0.05) in the distal colonic mucosa of rats fed tallow compared with soybean oil. Fecal bile acid concentrations were significantly lower in rats fed tallow compared with soybean oil. There were no significant differences in mucosal cell proliferation. No significant effects were found due to protein source or to interactions between fat and protein sources for ACF, cell proliferation labeling indexes, or bile acid concentrations. However, there was a significant protein by fat source interaction for the apoptotic labeling index. The decreased number of ACF, decreased fecal bile acid concentration, and increased mucosal apoptosis with tallow consumption are not consistent with a role for this fat in increasing risk of colon cancer.
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