Effect of the consumption of Lactobacillus coryniformis CECT5711 strain on the immune response of healthy adults

Among the various health-promoting functions of probiotics, much attention has been paid to their immunological function, although the immune response to probiotics is generally regarded to be strain dependent. For this purpose, the main objective of this study was to assess the effect of Lactobacillus coryniformis CECT5711 on the immune response of healthy adults during 6 weeks of treatment in a Hepatitis A vaccine model. One hundred twenty three volunteers were randomized into a placebo group, a probiotic group or a mixed group. Blood samples were taken at the beginning, after two weeks of treatment just before the vaccination and at the end of the study. Phagocytic and Natural Killer activities were measured in blood samples, besides the levels of cytokines using Luminex technology, leukocyte subsets assessed by monoclonal antibodies and specific Hepatitis A antibodies with a competitive ELISA.Sociedad Española de Probioticos y PrebioticosPeer Reviewe

Immune Development and Intestinal Microbiota in Celiac Disease

Celiac disease (CD) is an immune-mediated enteropathy, triggered by dietary wheat gluten and similar proteins of barley and rye in genetically susceptible individuals. The etiology of this disorder is complex, involving both environmental and genetic factors. The major genetic risk factor for CD is represented by HLA-DQ genes, which account for approximately 40% of the genetic risk; however, only a small percentage of carriers develop the disease. Gluten is the main environmental factor responsible for the signs and symptoms of the disease, but exposure to gluten does not fully explain the manifestation of CD. Epidemiological and clinical data suggest that environmental factors other than gluten might play a role in disease development, including early feeding practices (e.g., breast milk versus formula and duration of breastfeeding), infections, and alterations in the intestinal microbiota composition. Herein, we review what is known about the influence of dietary factors, exposure to infectious agents, and intestinal microbiota composition, particularly in early life, on the risk of developing CD, as well as the possible dietary strategies to induce or increase gluten tolerance

A Universal Approach to Eliminate Antigenic Properties of Alpha-Gliadin Peptides in Celiac Disease

Celiac disease is caused by an uncontrolled immune response to gluten, a heterogeneous mixture of wheat storage proteins, including the α-gliadins. It has been shown that α-gliadins harbor several major epitopes involved in the disease pathogenesis. A major step towards elimination of gluten toxicity for celiac disease patients would thus be the elimination of such epitopes from α-gliadins. We have analyzed over 3,000 expressed α-gliadin sequences from 11 bread wheat cultivars to determine whether they encode for peptides potentially involved in celiac disease. All identified epitope variants were synthesized as peptides and tested for binding to the disease-associated HLA-DQ2 and HLA-DQ8 molecules and for recognition by patient-derived α-gliadin specific T cell clones. Several specific naturally occurring amino acid substitutions were identified for each of the α-gliadin derived peptides involved in celiac disease that eliminate the antigenic properties of the epitope variants. Finally, we provide proof of principle at the peptide level that through the systematic introduction of such naturally occurring variations α-gliadins genes can be generated that no longer encode antigenic peptides. This forms a crucial step in the development of strategies to modify gluten genes in wheat so that it becomes safe for celiac disease patients. It also provides the information to design and introduce safe gluten genes in other cereals, which would exhibit improved quality while remaining safe for consumption by celiac disease patients

Factores inmunológicos de la leche materna

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Malnutrition and Inflammation

The relationship between nutrition and immune function is being widely recognized, although its study is relatively recent. The 1968 World Health Organisation monograph about “Interactions between Nutrition and Infection” presented the mechanisms linking infection and poor nutritional status. Following the development of immunology as a science, increasing evidence was obtained as well to show how undernutrition impaired resistance to infections and the immune response. It was initially recognized that deficits in certain micronutrients (like vitamins and minerals) had a direct impact on immune function. But the relationship between immune function and nutrition extends far beyond that, and the term immunonutrition has been coined. We are now aware of many conditions of nutritional imbalance (not all necessarily linked to nutritional deficiencies) that lead to impaired immune response. For instance, it is currently believed that nutrition is a key factor in the onset and development of many types of cancer, or that the dietary component of atherosclerosis risk can directly influence immune cells and the inflammatory response; certain nutrients, like seed and fish oils have been shown to respectively induce the release of pro- and anti-inflammatory mediators. Accordingly, the idea of undernutrition has been replaced by that of malnutrition, meaning that inappropriate nutrition or nutritional imbalance per se, whether it implies a nutrient deficit or not, influences immune function. That is the reason why overnutrition, or an excessive energy intake, is also now considered as malnutrition. In this chapter we will discuss three paradigmatic cases of malnutrition that have a strong immune and inflammatory impact: anorexia nervosa (AN) and bulimia nervosa (BN), as examples of severe undernutrition; obesity, also referred to as overnutrition; and celiac disease (CD), a pathological reaction of the body to a particular type of nutrients that leads to malnutrition. Although these nutrition-related diseases have different origins (psychological for eating disorders, modifiable lifestyle factors for obesity and autoimmune for CD), they all have in common to present an important inflammatory component and to have nutritional treatment as the main therapeutic approach.Peer Reviewe

Changes in gut microbiota due to supplemented fatty acids in diet-induced obese mice

Abstract Consumption of a high-fat diet (HFD), which is associated with chronic 'low-grade' systemic inflammation, alters the gut microbiota (GM). The aim of the present study was to investigate the ability of an oleic acid-derived compound (S1) and a combination of n-3 fatty acids (EPA and DHA, S2) to modulate both body weight and the GM in HFD-induced obese mice. A total of eighty mice were fed either a control diet or a HFD, non-supplemented or supplemented with S1 or S2. At week 19, faeces were collected in order to analyse the GM. Group-specific primers for accurate quantification of several major bacterial groups from faecal samples were assayed using quantitative PCR. The HFD induced an increase in body weight, which was reduced by supplementation with S1. Furthermore, S1 supplementation markedly increased total bacterial density and restored the proportions of bacteria that were increased (i.e. clostridial cluster XIVa and Enterobacteriales) or decreased (i.e. Bifidobacterium spp.) during HFD feeding. S2 supplementation significantly increased the quantities of Firmicutes (especially the Lactobacillus group). Correlation analysis revealed that body weight correlated positively with the phylum Firmicutes and clostridial cluster XIVa, and negatively with the phylum Bacteroidetes. In conclusion, the consumption of a HFD induced changes in the faecal microbiota, which were associated with the appearance of an obese phenotype. Supplementation of the HFD with S1 counteracted HFD-induced gut dysbiosis, together with an improvement in body weight. These data support a role for certain fatty acids as interesting nutrients related to obesity prevention.Peer Reviewe

Immunostimulatory effect of faecal Bifidobacterium species of breast-fed and formula-fed infants in a PBMC/CaCO-2 coculture system

Bifidobacterium spp. typical of the human intestinal microbiota are believed to influence the balance of immune responses in the intestinal mucosa. Aim: To investigate the effect of different bifidobacterial species and mixtures of them in in vitro experiments with PBMCs and CaCo-2 cells. Methods: Bifidobacterium adolescentis; Bifidobacterium angulatum; Bifidobacterium breve; Bifidobacterium catenulatum; Bifidobacterium infantis; Bifidobacterium longum; and two combinations of these bifidobacteria simulating the species composition found in fecal samples from breast fed (BF) and formula fed (FF) infants were used. The levels of several cytokines were measured by direct stimulation of PBMCs and by stimulation of a Caco-2/PBMCs co-culture with bifidobacteria. Results: B. catenulatum and B. breve were the strongest enhancers of IFN-γ, production by direct stimulation of PBMCs. B. longum was the highest inducer of IL-10 and the lowest TNF-α stimulus. In the Caco-2/PBMC system, B. breve was the highest inducer of IL-8 production by Caco-2 cells; significantly different from B. infantis, B. adolescentis and the FF mixture (p<0·05). IFN-γ produced by PBMCs stimulated with the BF mixture (containing 22% B. breve, compared to 7% in FF mixture) was significantly higher compared to B. adolescentis, B. infantis, and B. longum. B. adolescentis also inhibited IFN-γ production compared to FF mixture and B. longum. Conclusions: The proportion of different Bifidobacterium strains seems to be an important determinant of the cytokine balance in the simulated intestinal environment studied. B. breve and the combination of the Bifidobacterium species typically found in the microbiota of breast-fed infants have shown the most significant effects.Peer reviewe

Influence of beverages characteristics on the drinking pattern and on the hydration status

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Estrategias dietéticas de inmunomodulación en niños con riesgo de padecer enfermedad celiaca

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