Improving knowledge about breast cancer etiology is crucial in order to propose prevention strategies for this pathology. Gut microbiota is involved in numerous physiopathological situations including cancers. Although its potential involvement in breast cancer through the alteration of the enterohepatic circulation of estrogens and/or the metabolism of phytoestrogens has been discussed for some time, it remains to be demonstrated. The present study seeks to strengthen this hypothesis by identifying possible links between the fecal microbiota composition and clinical characteristics in breast cancer patients. Bacterial DNA was extracted from the feces of 31 patients with early-stage breast cancer and amplified by real-time polymerase chain reaction (qPCR), targeting 16S rRNA sequences specific to bacterial groups, and then analyzed in relation to clinical characteristics. The absolute numbers of total bacteria and of three bacterial groups (Firmicutes, Faecalibacterium prausnitzii, and Blautia) differed significantly according to the patient's body mass index. The percentage and the absolute numbers of certain bacterial groups, namely C. coccoides, F. prausnitzii, and Blautia, differed significantly according to the clinical stages and the histoprognostic grades. Our study highlighted that intestinal microbiota composition in these patients differs according to clinical characteristics and BMI. Further studies are required to clarify the link between breast cancer and intestinal microbiota.

Fructooligosaccharides (FOS) increase the growth of lactic acid bacteria (LAB) and promote butyrate and lactate production. Because of these properties, FOS may benefit intestinal inflammation. The purpose of this study was to investigate the effect of FOS on colitis in rats and determine which factors are involved. Groups of rats with intracolonic trinitrobenzene sulfonic acid (TNBS)-induced colitis received intragastric infusions of 9 g/L NaCl, 1 g/d FOS or 10(11) colony-forming units (cfu)/d LAB (Experiment 1), or intracolonic infusions of 9 g/L NaCl, butyrate, lactate or butyrate + lactate with or without 10(9.5) cfu/d LAB (Experiment 2). Each infusion was administered twice daily for 14 d. Intragastric FOS reduced the gross score for inflammation (P < 0.001), myeloperoxidase (MPO) activity (P < 0.001) and pH (P < 0.001), and increased lactate (P = 0.02) and butyrate concentrations (P < 0.001) as well as LAB counts in the cecum (P < 0.01). Intragastric LAB (10(11) cfu/d) had the same beneficial effects as FOS and modified the cecal composition similarly. High doses of intracolonic butyrate and lactate reduced the indices of inflammation (P < 0.001), whereas administration of the lower concentrations found in the colon tended to decrease (P < 0.1) the gross score for inflammation and MPO activity. Addition of LAB (10(9.5) cfu/d) to the organic acids was necessary to reproduce the significant FOS-induced effects on these variables. Thus, under the experimental conditions used, FOS reduced intestinal inflammatory activity mainly by increasing LAB counts in the intestine.

We showed that IUGR induced, per se, some neonatal and long-lasting alterations of the intestinal microbiota. The physiological consequences of these changes and their relation to the predisposing effect of IUGR to gut pathologies must now be explored.

The ovine embryo produces an interferon named ovine Trophoblastin (oTP) which is involved in the maternal recognition of pregnancy and ensures the maintenance of progesterone secretion by the corpus luteum. We have used indirect immunohistofluorescence and in situ hybridization on histological sections to investigate the fate of this protein and its mRNA in ovine embryos from days 3 to 25 of pregnancy. The level of expression was measured by image analysis of the autoradiographs after in situ hybridization. Both techniques clearly demonstrated that oTP and its mRNA were specifically localized in the extra-embryonic trophoblast. Neither the embryonic cells, nor the yolk sac or the amniotic tissues produced the protein or its mRNA. The protein could be detected by d 11 of pregnancy in the elongated blastocyst. Maximum of expression is observed at d 14 and the level decreased by d 16 of pregnancy. The arrest of expression occurred in the regions of trophoblast which have established cellular contacts with the uterine epithelium during the implantation process.