1. Lymphocyte Transformation of Peripheral Blood Lymphocytes
2. Plaque-forming Cell of the Splenic and the Nucleated Cells of the Mesen-teric Lymph Nodes
3. Serum Concentration of α -Fetoprotein and Albumin
4. Suppression of Immunoresponse in the Suckling Piglet
5. Influence of Immunopotentiator on Suckling Piglets
Influence of Peptidoglycan on Lymphocyte Transformation
Influence of Peptidoglycan on Immunoglobulin IgA-bearing Cells in the Lamina
Propria of the Small Intestine
6. Influence of Peptidoglycan on the Incidence of Pig Scour

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Enterococcus faecalis BIO-4R (BIO-4R) showed a decreased growth rate in ACY broth as compared with its parental strain, BIO, but both the strains attained a maximal level of viable cell number of about 10^8.5 per ml. In “ feces medium ” BIO-4R reached maximal concentration of about 10^7.4 cells per ml after 24 hr of incubation. When inoculated with Bacillus subtilis (natto) in the continuous flow culture, the growth of BIO-4R was fairly enhanced. On the other hand, BIO-4R with Candida albicans resulted in a marked suppression of C. albicans. BIO-4R was developed in the intestinal tract of gnotobiotic mice at levels of about 10⁸ cells per g feces after oral administration. In the intestine of conventional mice, BIO-4R hardly grows but did moderately in mice which were treated with antibiotics such as streptomycin plus erythro-mycin. When administered orally to piglets, BIO-4R appeared to suffer a decrease in the number of viable cells while passing through the acidic part of the stomach and duodenum, and the BIO-4R may grow again to some extent in the ileum. In calves, BIO-4R was detectable at only low levels in feces after the oral administration. In both piglets and calves, lactic flora such as bifidobacteria, streptococci, and lactobacilli was enhanced, and putrefactive organisms as Salmonella and yeasts were suppressed by administering with BIO-4R. In humans BIO-4R was able to be detected in stools of all the subjects given more than 10⁷ cells of the organism. The dose of over 10⁷ cells was required to prevent infants from the incidence of thrush during antibiotic therapy. These results suggest that intestinal flora may interfere with BIO -4R and the BIO-4R would not stably colonize the intestine of human and animals. BIO-4R, however, may multiply to some extent in the intestine in which the normal microbialflora was eliminated.

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For the purpose of investigating the effects of Biofermin-R (BF-R) on the bacterial flora, BF-R was administered in combination with antibiotics, and the fecal flora of children treated with antibiotics alone was compared with that of children treated with both BF-R and antibiotics. Three types of effects were investigated: 1) the inhibitory effect on antibiotic-induced changes of the bacterial flora in patients without diarrhea, 2) the bacterial flora-maintaining and normalizing effect in patients with gastrointestinal symptoms, and 3) the process of normalizing in the fecal bacterial flora of mice administered with antibiotics. The results indicated that the concurrent use of BF-R and an antibiotic inhibited the changes of the intestinal flora that usually occur during antibiotic therapy alone, by preventing a decrease in Bifidobacterium, and restored disturbed flora to normal.

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The effects of feeding sour milk on longevity, transplantable tumor, and chemically induced colon tumorigenesis were studied.(1) Female ICR mice were fed with pasteurized sour milk throughout their life. Mice given sour milk had a longer life span than those given the control diet, while the life span of those given whole milk was almost the same as those given the control diet. Necropsy showed that the main causes of death were tumors, renal atrophy, and pneumonia. Sour milk was suggested to inhibit at least one of these diseases.(2) Female ICR mice were intraperitoneally inoculated with Ehrlich ascites tumor cells, and the effect of dietary sour milk on the growth of tumor cells was determined. Feeding pasteurized sour milk or pasteurized starter cells inhibited the growth of tumor cells. The inhibitory effect was dependent on the dose of the starter cells. These results suggested that some component (s) of starter cells was responsible for inhibition of tumor cell proliferation.(3) When male F344 rats were intraperitoneally injected with 1, 2-dimethylhydrazine, the effect of dietary sour milk on the incidence of intestinal tumors induced was studied. While the number of colon tumors per animal in rats fed with artificially acidified milk or starter cells was not significantly different from that in rats fed with control diet, rats fed with sour milk developed significantly fewer colon tumors. This finding indicates that sour milk inhibited 1, 2-dimethylhydrazine-induced colon tumorigenesis in F344 rats.

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