We estimated the density of TMC0356 to be over 105 CFU per 1 g of feces. Moreover, when TMC0356F-100 was subcultured repeatedly in skim milk, and then digested with ApaI, TMC0356F-100 and TMC0356 were different from each other in two bands on PFGE. However, no difference between TMC0356F-100 and TMC0356 could be detected by carbohydrate fermentation and enzymatic activity tests (data not shown). These results indicate that there are some changes in the genome of TMC0356 after repeated reculture, although
these changes do not alter tested physiological functions of this bacterium. Therefore, the method developed in the present study might be, at least partly, dependent on the frequency of subculturing. TMC0356 can be MK-2206 mouse distinguished from other strains by PFGE using three restriction enzymes—SmaI, SacII, and ApaI. PFGE is also useful for the detection of L. gasseri TMC0356 in human feces.
Our results indicate that orally administered TMC0356 can survive in, and colonize, the human intestine. We thank Professor Hisakazu Iino (Life Science for Living System, Graduate School, Showa Women’s University) for isolation and identification of lactobacilli in the fecal samples of our subjects. We also thank Professor Takao Mukai (School of Veterinary Medicine, Kitasato University) for technical advice relating to PFGE. This work was supported by a Grant-in-Aid for Research and Development from the Japanese Ministry of Agriculture and Forestry. “
“Intraperitoneal larval infection (alveolar PLX-4720 mouse echinococcosis, AE) with Echinococcus multilocularis in mice impairs host immunity. Metacestode metabolites may modulate immunity putatively 4��8C via dendritic cells. During murine AE, a relative increase of peritoneal DCs (pe-DCs) in infected mice (AE-pe-DCs; 4% of total peritoneal cells) as compared to control mice (naïve pe-DCs; 2%) became apparent in our study. The differentiation of AE-pe-DCs into TGF-β-expressing cells and the
higher level of IL-4 than IFN-γ/IL-2 mRNA expression in AE-CD4+pe-T cells indicated a Th2 orientation. Analysis of major accessory molecule expression on pe-DCs from AE-infected mice revealed that CD80 and CD86 were down-regulated on AE-pe-DCs, while ICAM-1(CD54) remained practically unchanged. Moreover, AE-pe-DCs had a weaker surface expression of MHC class II (Ia) molecules as compared to naïve pe-DCs. The gene expression level of molecules involved in MHC class II (Ia) synthesis and formation of MHC class II (Ia)–peptide complexes were down-regulated. In addition, metacestodes excreted/secreted (E/S) or vesicle-fluid (V/F) antigens were found to alter MHC class II molecule expression on the surface of BMDCs.