Health claims of lactic acid bacteria (LAB) used in functional foods and pharmaceutical preparations are based on the capacity of these microorganisms to stimulate the host immune system. In this study, the antigenic effect of LAB (Lactobacillus acidophilus, Lactobacillus casei, Lactobacillus delbrueckii ssp. bulgaricus and Streptococcus thermophilus) on the gut immune system of BALB=c mice was evaluated. A dose-dependent increase of the Bcl2 protein was observed with all LAB assayed. Furthermore, the analysis of cytokine-producing cells in the lamina propria of gut showed that TNFa and INFg values, determined in macrophages cultured from Peyer patches, were enhanced for all the LAB assayed. An important increase of interleukins IL-10 and IL-4 was observed mainly in mice fed with Lactobacillus delbrueckii ssp. bulgaricus or Lactobacillus casei, while a significant induction of IL-2 and IL-12 was only observed with L. acidophilus (P < 0.01). These effects were dose dependent. The role of produced cytokines in the balance Th1=Th2 was determined by a systemic antibody response against parenterally injected ovoalbumin. L. casei, L. delbrueckii ssp. bulgaricus and L. acidophilus enhanced the IgG1 response favouring Th2 balance, while L. acidophilus also increased the IgG2a response inducing Th1 balance. S. thermophilus did not influence the balance Th1=Th2. Our studies showed that lactic acid bacteria induce distinct mucosal cytokine profiles showing different adjuvant capacity among them. Thus, selection of probiotic strain with immunological properties must be well defined to influence cytokine expression that favour the claimed immune response.

The induction of a mucosal immune response is not easy due to the development of oral tolerance, but under some conditions, bacteria can activate this immune system. Antigens administered orally can interact with M cells of Peyer's patches or bind to the epithelial cells. We have demonstrated that certain lactic acid bacteria are able to induce specific secretory immunity, and others will enhance the gut inflammatory immune response. The aim of this work was to establish the reason for these different behaviors and to define possible mechanisms involved in the interaction of lactic acid bacteria at the intestinal level. We studied IgA+ and IgM+ B cells comparatively in bronchus and intestine and CD4+ T cells and IgA anti-lactic acid bacteria antibodies in the intestinal fluid, induced by oral administration of Lactobacillus casei, Lb. delbrueckii ssp. bulgaricus, Lb. acidophilus, Lb. plantarum, Lb. rhamnosus, Lactococcus lactis, and Streptococcus salivarius ssp. thermophilus. The increase in the IgA+ B cells in the bronchus means that these lactic acid bacteria were able to induce the IgA cycle by interaction with M cells from Peyer's patches or intestinal epithelial cells. The IgM+ cells increased when the stimulus did not induce the switch from IgM+ to IgA+. The increase in the CD4+ cells suggests interaction of Peyer's patches and enhancement of the B- and T-cell migration. The anti-lactic acid bacteria antibody is related to the processing and presentation of the microorganisms to the immune cells. We demonstrated that Lb. casei and Lb. plantarum were able to interact with Peyer's patch cells and showed an increase in IgA-, CD4+ cells, and antibodies specific for the stimulating strain. Lactobacillus acidophilus induced gut mucosal activation by interaction with the epithelial cells without increase in the immune cells associated with the bronchus. Although Lb. rhamnosus and Strep. salivarius ssp. thermophilus interact with epithelial cells, they also induced an immune response against their epitopes. Lactococcus lactis and Lb. delbrueckii ssp. bulgaricus induced an increase of IgA+ cells entering the IgA cycle but not CD4+ cells; thus, these bacteria would have been bound to epithelial cells that activated B lymphocytes without processing and presenting of their epitopes. We did not determine specific antibodies against Lc. lactis or Lb. bulgaricus.

In patients treated with a single injection of palonosetron on day 1, reducing dexamethasone is an option that is not associated with significant reduction in antiemetic control during the 5-day period or an impact on patient functioning.

Swiss Albino mice were fed a diet enriched with fat to produce hypercholesterolemia. The further administration of Lactobacillus reuteri CRL 1098 (10(4) cells/d) to hypercholesterolemic mice for 7 d decreased total cholesterol by 38%, producing serum cholesterol concentrations similar to that of the control group (67.4 mg/ml). This low dose of L. reuteri caused a 40% reduction in triglycerides and a 20% increase in the ratio of high density lipoprotein to low density lipoprotein without bacterial translocation of the native microflora into the spleen and liver. These data suggest that L. reuteri CRL 1098 is an effective hypocholesterolemic adjuvant at a low cell concentration for mice.

CTCs basal value is a predictive indicator of prognosis and changes in CTC levels during therapy may indicate a clinical response. Testing CTC levels during targeted treatments might substitute other measurement parameters for response evaluation.

Aims: To investigate whether there is a relationship between interaction sites in the gut, hydrophobicity, mucosal immunomodulating capacities and cell wall protein profiles in lactobacilli, bifidobacteria and enterococci. Methods and Results: Hydrophobicity, cell wall protein profiles and sites of interaction in the gut (by using fluorescein isothiocyanate-labelled bacteria) were determined for Lactobacillus casei, L. acidophilus, L. fermentum, Bifidobacterium bifidum, B. animalis and Enterococcus faecalis. We also determined the number of immunoglobulin (Ig)A + , tumour necrosis factor (TNF)a + , interleukin (IL)-6 + and IL-10 + cells after oral administration of the above bacteria to BALB/c mice. All strains assessed were found to interact with the sites of induction of the immune response in the gut. No correlation with hydrophobicity was observed. When some strains at certain doses were administered to mice, bacterial translocation to liver was observed. The oral administration of indigenous (10 4 cells day )1 ) and exogenous (10 7 cells day )1 ) bifidobacteria and lactobacilli for 5 consecutive days activated the systemic and intestinal mucosal immune response in a strain-specific way, independently whether the strain was indigenous or exogenous in relation to the host. The differences in the immunopotentiating capacity of the various strains might be related to the differences in their cell wall protein profiles. Conclusions: Indigenous bacteria activated the mucosal immune response at a dose significantly smaller than the one required for probiotic exogenous bacteria. However, probiotic exogenous bacteria can be used at high concentrations in fermented dairy products with a great impact on the immune system, favouring its immunomodulation.Significance and Impact of the Study: The immunomodulation capacity of probiotic bacteria is strain specific and independent of the specificity of the host. The ability of certain strains to down-regulate the production and release of IL-6 by IL-10 may have potential implications in their use in cases in which cytokine deregulation or excessive production at the mucosal level can be the cause of tissue damage.

Administration of Lactobacillus reuteri CRL 1098 (10(4) cells/d) to mice for 7 d before inducing hypercholesterolemia (by feeding mice with a fat-enriched diet for the subsequent 7 d) was evaluated. At this low dose, L. reuteri was effective in preventing hypercholesterolemia in mice, producing a 17% increase in the ratio of high-density lipoprotein to low-density lipoprotein. Total cholesterol and triglycerides decreased by 22 and 33%, respectively, in the group that was not fed the lactobacilli. The hypocholesterolemic effect produced by L. reuteri CRL 1098 might be considered as indirect evidence of the permanency of the lactobacilli in the gut.

Background: Patients invited to take part in a clinical trial may evoke an archetype on which they may base their decision of adherence to participation, instead of on the study itself. Methods: A 17-item, multiple choice questionnaire was developed, tested and then administered to 102 Italian-speaking patients with advanced lung or breast cancers who had never been exposed to participation in a trial. Results: The questionnaire was answered by all patients. Eighty-five percent were positive about trial participation. Demographic factors did not influence patients’ willingness to participate. Trust in the investigator (76%) or in the institute (64%) and hope of receiving a new chance for cure (78%) were cited as reasons to accept participation. A minority was concerned by potential conflicts of interest (31%) or the thought of being ‘guinea pigs’ (36%), and feared that doctors were interested in advancing their own research, even though there were more efficient drugs available (28%). Fifty percent feared receiving a little-known medicine, and 76% considered that a thorough explanation of toxicity/safety of the proposed treatment helped them decide. Conclusion: Several prejudices, fears and some hopes have been captured by the questionnaire. Understanding such specifics will improve patient information leading patients to a more conscious motivation in deciding whether to participate in a clinical trial.