Celiac disease-specific prolamin peptide content of wheat relatives and wild species determined by ELISA assays and bioinformatics analyses

Enzyme-linked immunosorbent assays (ELISAs) are widely used to determine gluten contamination in gluten-free and low gluten food samples. ELISA assays developed using monoclonal antibodies against known toxic peptides have an advantage in the identification of toxic prolamin content in protein extracts of different food samples, as well as raw materials. R5 and G12 monoclonal antibodies specific for two known toxic peptides used in commercially available gluten ELISA assays were applied to test toxic peptide contents in wheat relatives and wild wheat species with different genome composition and complexity. Although the R5 peptide content showed some correlation with ploidy levels in Triticum species, there was a high variance among Aegilops species. Some of the analysed diploid Aegilops species showed extremely high R5 peptide contents. Based on the bioinformatics analyses, the R5 peptide was present in most of the sulphur rich prolamins in all the analysed species, whereas the G12 epitope was exclusively present in alpha gliadins. High variation was detected in the position and frequency of epitopes in sequences originating from the same species, thus highlighting the importance of genotypic variation within species. Identification of new prolamin alleles of wheat relatives and wild wheat species is of great importance in order to find germplasm for special end-use quality purposes as well as development of food with reduced toxicity

Towards breeding less allergenic spelt-wheat with low fodmap content — A review

Consumption of “gluten-containing” diet causes disease for a significant minority of people who consume foods derived from wheat, rye, barley, and possibly oat. The fact is, however, that in several types of diseases related to the consumption of “gluten-containing” cereals, the trigger compounds are not components of gluten. The current view of medical experts is that, excluding people suffering from celiac disease, the majority of individuals who are feeling better on the “wheat-free” or “gluten-free” diet could select a food containing much healthier, low level of fermentable oligosaccharides (often called as FODMAP). To satisfy the specific health related demands of certain consumer groups, the challenge is in front of cereal breeding to develop new, “healthier” germplasms, suitable to produce such products by the food industry. This report aims to give an overview of some aspects of recent developments in this booming area, (i) summarizing the up-to-date knowledge on cereals-related health disorders; (ii) reporting on the status of developing celiac-safe cereals, and finally (iii) highlighting the potential of developing “healthier” spelt-based cereal products through the progress in an ongoing spelt breeding program

Measurement of cross sections and leptonic forward-backward asymmetries at the Z pole and determination of electroweak parameters

We report on the measurement of the leptonic and hadronic cross sections and leptonic forward-backward asymmetries at the Z peak with the L3 detector at LEP. The total luminosity of 40.8 pb −1 collected in the years 1990, 1991 and 1992 corresponds to 1.09·10 6 hadronic and 0.98·10 5 leptonic Z decays observed. These data allow us to determine the electroweak parameters. From the cross sections we derive the properties of the Z boson: assuming lepton universality. We obtain an invisible width of Γ inv =496.5±7.9 MeV which, in the Standard Model, corresponds to a number of light neutrino species of N v =2.981±0.050.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47894/1/10052_2005_Article_BF01574160.pd

Mechanisms of allergic contact dermatitis

Allergenicity depends on several factors determined by the very physicochemical nature of the molecules themselves, i.e., their capacity to penetrate the horny layer, lipophilicity, and chemical reactivity. The sensitizing property of the majority of contact allergens could be predicted from these characteristics (Patlewicz et al., Contact Dermatitis 50:91-97, 2004; Gerberick et al., Altern Lab Anim 36(2):215-242, 2008). Two other factors, however, further contribute to the allergenicity of chemicals, namely, their pro-inflammatory activity and capacity to induce maturation of LC. These issues will be dealt with in more detail in the following sections. Along with their migration and settling within the draining lymph nodes, haptenized LC further mature, as characterized by their increased expression of costimulatory and antigen-presentation molecules (Cumberbatch et al., Arch Dermatol Res 289:277-284, 1997; Heufler et al. J Exp Med 167:700-705, 1988). In addition, they adopt a strongly veiled, interdigitating appearance, thus maximizing the chances of productive encounters with naive T lymphocytes and recognition of altered self (Steinman et al., J Invest Dermatol 105:2S-7S, 1995; Furue et al., Br J Dermatol 135:194-198, 1996; Schuler and Steinman, J Exp Med 161:526-546, 1985). The intricate structure of lymph node paracortical areas, the differential expression of chemokines and their receptors, the characteristic membrane ruffling of IDC, and the predominant circulation of naive T lymphocytes through these lymph node areas provide optimal conditions for T-cell-receptor binding, i.e., the first signal for induction of T-cell activation (Banchereau and Steinman, Nature 392:245-252, 1998). Intimate DC-T-cell contacts are further strengthened by secondary signals, provided by sets of cellular adhesion molecules, and growth-promoting cytokines (reviewed in Hommel, Immunol Cell Biol 82:62-66, 2004; Cella et al., Curr Opin Immunol 9:10-16, 1997). In healthy individuals, primary skin contacts with contact allergens lead to differentiation and expansion of allergen-specific effector T cells displaying Th1, Th2, and/or Th17 cytokine profiles. The same allergens, if encountered along mucosal surfaces, favor the development of allergen-specific Th2 and Th17 effector cells, and/or Th3 and Tr1 allergen-specific regulatory T cells. Whereas the first two subsets may assist or replace Th1 cells in pro-inflammatory effector functions, the latter two subsets are mainly known for downregulating immune responsiveness. For most, if not all allergens, along with prolonged allergenic contacts, the role of Th2 cells as effector cells gradually increases given reduced longevity of Th1 responses. The respective contributions of similar subsets of allergen-specific CD8 + T cells are still unknown, but distinct effector roles of allergen-specific Tc1 and Tc2 have been postulated. Priming via the skin results in CLA positive T cells, which upon inflammatory stimuli preferentially enter the skin; on the other hand, gut homing T cells have been primed and generated along mucosal surfaces. Upon priming, T cells loose much of their capacity to recirculate via the lymph nodes, but gain the capacity to enter the tissues. In particular recently activated T cells will enter skin inflammatory sites. ACD reactions are primarily infiltrated by CD4 and/or CD8 pro-inflammatory cells, later reactions may be dominated by Th2 cells and regulatory T cells. Skin infiltation by T cells is fine-tuned by sets of adhesion molecules and chemokine receptors, whose expression is not rigid, but can be modulated by micro-environmental factors. After antigenic activation the progeny of primed T cells is released via the efferent lymphatics into the bloodstream. Circulating allergen-specific cells can be challenged in vitro to provide diagnostic parameters for contact hypersensitivity. At least for water-soluble allergens, like metal salts, the degree of allergen-specific proliferation and cytokine production, in particular type-2 cytokines, correlate with clinical allergy. For routine application of a broad spectrum of allergens, culture conditions still need to be improved. For mechanistic in vitro studies in ACD, however, with selected sets of relatively nontoxic allergens, peripheral blood provides an excellent source of lymphocytes and antigen-presenting cells. ACD reactions can be mediated by classical effector cells, i.e., allergen-specific CD4+ type-1 T cells which, upon triggering by allergen-presenting cells, produce IFN-? to activate nonspecific inflammatory cells like macrophages. However, CD8 + T cells, and other cytokines, including IL-4, IL-17, and IL-22 can also play major roles in ACD. The conspicuous difference with DTH reactions induced by intradermal administration of protein antigens, i.e., the epidermal infiltrate, can largely be attributed to hapten-induced chemokine release by keratinocytes