Supplementation with Lactobacillus reuteri or L. acidophilus reduced intestinal shedding of cryptosporidium parvum oocysts in immunodeficient C57BL/6 mice.

The effect of L. acidophilus supplementation to reduce fecal shedding of Cryptosporidium parvum oocysts was compared to L. reuteri using C57BL/6 female mice immunosuppressed by murine leukemia virus (strain LP-BM5) inoculation. After 12 weeks post LP-BM5 inoculation, 15 immunosuppressed mice each were randomly assinged to one of the following treatment groups: historical control (group A), LP-BM5 control (group B), C. parvum (group C), L. reuteri plus C. parvum (group D) or L. acidophilus plus C. parvum (group E). Mice were pre-fed the L. reuteri or L. acidophilus bacteria strains daily for 13 days, challenged with C. parvum oocysts and thereafter fed the specified Lactobacillus regimens daily during the experimental period. Animals supplemented with L. reuteri shed fewer (p<0.05) oocysts on day-7 post C. parvum challenge compared to controls. Mice supplemented with L. acidophilus also shed fewer (p<0.05) oocysts on days 7 and 14 post-challenge compared to controls. Overall, Lactobacillus supplementation reduced C. parvum shedding in the feces but failed to suppress the production of T-helper type 2 cytokines [interleukin-4 (IL-4), IL-8)] which are associated with immunosuppression. Additionally, Lactobacillus supplementation did not restore T-helper type 1 cytokines (interleukin-2 (IL-2) and gamma interferon (IFN-gamma), which are required for recovery from parasitic infections. Altered T-helper types 1 and 2 cytokine production as a consequence of immunodysfunction permitted the development of persistent cryptosporidiosis while mice with intact immune system were refractory to infection with C. parvum. Reduction in shedding of oocysts observed in the Lactobacillus supplemented mice during deminished IL-2 and IFN-gamma production may be mediated by factors released into the intestinal lumen by the Lactobacillus and possibly other host cellular mechanisms. These observations suggest that L. reuteri or L. acidophilus can reduce C. parvum parasite burdens in the intestinal epithelium during cryptosporidiosis and may serve potential benefits as probiotics for host resistance to intestinal parasitic infections. L. acidophilus was more efficacious in reducing fecal shedding than L. reuteri and therefore may also have implication in the therapy of cryptosporidiosis during immunosuppressive states including human AIDS.

Effect of Lactobacillus reuteri on intestinal resistance to Cryptosporidium parvum infection in a murine model of acquired immunodeficiency syndrome.

Efficacy of Lactobacillus reuteri as a probiotic for the control of Cryptosporidium parvum infection was evaluated in C57BL/6 female mice that were immunosuppressed by intraperitoneal inoculation with the LP-BM5 leukemia virus. Four months after inoculation, mice developed lymphadenopathy, splenomegaly, and susceptibility to C. parvum infection. After daily prefeeding with L. reuteri (10(8) cfu/day) for 10 days, mice were challenged with 6.5 x 10(6) C. parvum oocysts and fed L. reuteri during the entire study. Mice supplemented with L. reuteri and challenged with C. parvum cleared parasite loads from the gut epithelium. However, unsupplemented animals developed persistent cryptosporidiosis and shed high levels of oocysts in the feces. L. reuteri feeding increased its colonization of the intestinal tract, which was inversely related to the fecal shedding of oocysts. These findings suggest that L. reuteri may help prevent C. parvum infection in immunodeficient subjects.

Enhancement of resistance to Cryptosporidium parvum by pooled bovine colostrum during murine retroviral infection.

The therapeutic efficacy of pooled bovine colostrum for the control of cryptosporidiosis was investigated during murine acquired immunodeficiency syndrome in female C57Bl/6 mice. Mice were infected with LP-BM5 murine leukemia retrovirus for four months and then inoculated with Cryptosporidium parvum oocysts. Persistent cryptosporidiosis was established in all retrovirus immunosuppressed mice, while control mice were refractory to infection. Parasite colonization of intestinal villi was significantly (P < 0.05) reduced in immunosuppressed animals that received dietary supplemental pooled bovine colostrum compared with to those that did not receive colostrum treatment. Similarly, shedding of oocysts in the feces of immunosuppressed animals that received dietary pooled bovine colostrum was significantly (P < 0.05) reduced compared with those that did not at 26 days post-parasite challenge. Since the nonimmune bovine colostrum contained no anti-Cryptosporidium antibodies, this suggests that passively transferred antibodies alone are unlikely to have provided the improved resistance shown in this study.

The effect of vitamin E (alpha-tocopherol) supplementation on hepatic levels of vitamin A and E in ethanol and cod liver oil fed rats.

Eight groups of 5 rats were fed 8 differing liquid diets with and without ethanol, cod liver oil and/or increased levels of vitamin E. Hepatic levels of vitamins A and E were determined following the 28-day feeding time. Ethanol consumption decreased the levels of hepatic vitamin E (p less than 0.05), vitamin A (p less than 0.05) and the ratio of vitamin A/E (p less than 0.05). Hepatic levels of vitamins A and E were unaffected in rats fed cod liver oil. Supplementation of the normal dietary level of 30 IU of vitamin E per kg diet, with an additional 142 IU alpha tocopherol/kg diet, restored hepatic concentrations of vitamin E to normal levels in alcohol-fed rats. The hepatic levels of vitamin A in rats fed ethanol diets supplemented with vitamin E were less than that of control rats but were 4.3 times greater than that of rats on ethanol diets unsupplemented with vitamin E. However, the vitamin A and E ratio was equal to normal in this group of rats. The vitamin A/E ratio was reduced in liver of rats fed non-alcoholic diets supplemented with vitamin E due to increased levels of hepatic vitamin E. Additionally, rats fed cod liver oil diets containing ethanol also indicated decreased hepatic vitamin A and E levels. However, these levels were greater than that of rats fed only alcoholic diets suggesting that these vitamins are replaced by the vitamin A and E content in the cod liver oil.(ABSTRACT TRUNCATED AT 250 WORDS)