Building Valorisation Strategies for Biodiverse Products - Case Studies

The market valorisation of ‘diverse food products’ is crucial to promote agrobiodiversity. Despite the differences due to the specific contexts, valorisation strategies show relevant common features

Building valoristaion strategies for biodiverse products - the approach

The market valorisation of ‘diverse food products’ is crucial to increase diversity in farming systems. It involves multiple actors, from the field to the table, and requires an integrated approach to take into account several dimensions involved

Cultivating diversity and food quality. Proceedings of Diversifood EU Forum, Brussels, 11 April 2018

To tackle this issue, Diversifood team organised a forum with policy makers and stakeholders on the 11th of April 2018, in Brussels. Diversifood’s aim is to share results and key lessons including new approaches for the management of cultivated biodiversity, for plant breeding for sustainable farming systems, and new relationships among actors of food systems. In the afternoon, there was time for discussion, knowledge sharing, collecting feedback and extending current policies to include cultivating diversity and food quality (for FP9, CAP 2020, The outputs of this workshop will feed Diversifood’s final recommendations. The forum was kindly hosted by the European Committee of the Regions (Rue Belliard/Belliardstraat 101, 1040 Brussels)

High-resolution maps of Swiss apiaries and their applicability to study spatial distribution of bacterial honey bee brood diseases

Honey bees directly affect and are influenced by their local environment, in terms of food sources, pollinator densities, pathogen and toxin exposure and climate. Currently, there is a lack of studies analyzing these data with Geographic Information Systems (GIS) to investigate spatial relationships with the environment. Particularly for inter-colonial pathogen transmission, it is known that the likelihood of a healthy colony to become infested (e.g., Varroosis) or infected (e.g., American foulbrood—AFB, European foulbrood—EFB) increases with higher colony density. Whether these transmission paths can actually be asserted at apiary level is largely unknown. Here, we unraveled spatial distribution and high-resolution density of apiaries and bacterial honey bee brood diseases in Switzerland based on available GIS data. Switzerland as ‘model country’ offers the unique opportunity to get apiary data since 2010 owing to compulsory registration for every beekeeper. Further, both destructive bee brood diseases (AFB and EFB) are legally notifiable in Switzerland, and EFB has an epizootic character for the last decades. As governmental data sets have to be ameliorated, raw data from the cantonal agricultural or veterinary offices have been included. We found a mean density of 0.56 apiaries per km2, and high resolution spatial analyzes showed strong correlation between density of apiaries and human population density as well as agricultural landscape type. Concerning two bacterial bee brood diseases (AFB, EFB), no significant correlation was detectable with density of apiaries on cantonal level, though a high correlation of EFB cases and apiary density became obvious on higher resolution (district level). Hence, Swiss EFB epizootics seem to have benefited from high apiary densities, promoting the transmission of pathogens by adult bees. The GIS-based method presented here, might also be useful for other bee diseases, anthropogenic or environmental factors affecting bee colonies

CD103 Deficiency Prevents Graft-versus-Host Disease but Spares Graft-versus-Tumor Effects Mediated by Alloreactive CD8 T Cells

Graft-versus-host disease (GVHD) remains the main barrier to broader application of allogeneic hematopoietic stem cell transplantation (alloSCT) as a curative therapy for host malignancy. GVHD is mediated by allogeneic T cells directed against histocompatibility antigens expressed by host tissues. Based on previous studies, we postulated that the integrin CD103 is required for CD8-mediated GVHD, but not for graft-versus-tumor effects (GVT).We herein provide evidence in support of this hypothesis. To circumvent the potentially confounding influence of donor CD4 T cells, we developed an alloSCT model in which GVHD mortality is mediated by purified CD8 T cells. In this model, host-reactive CD8 T cells receive CD4 T cell help at the time of initial activation but not in the effector phase in which mature CD8 T effectors migrate into host tissues. We show that donor CD8 T cells from wild-type BALB/c mice primed to host alloantigens induce GVHD pathology and eliminate tumors of host origin in the absence of host CD4 T cells. Importantly, CD103 deficiency dramatically attenuated GVHD mortality, but had no detectable impact on the capacity to eliminate a tumor line of host origin. We provide evidence that CD103 is required for accumulation of donor CD8 T cells in the host intestinal epithelium but not in the tumor or host lymphoid compartments. Consistent with these data, CD103 was preferentially expressed by CD8 T cells infiltrating the host intestinal epithelium but not by those infiltrating the tumor, lamina propria, or lymphoid compartments. We further demonstrate that CD103 expression is not required for classic CD8 effector activities including cytokine production and cytotoxicity.These data indicate that CD103 deficiency inhibits GVHD pathology while sparing anti-tumor effects mediated by CD8 T cells, identifying CD103 blockade as an improved strategy for GVHD prophylaxis

Killing of Targets by CD8+ T Cells in the Mouse Spleen Follows the Law of Mass Action

It has been difficult to correlate the quality of CD8 T cell responses with protection against viral infections. To investigate the relationship between efficacy and magnitude of T cell responses, we quantify the rate at which individual CD8 effector and memory T cells kill target cells in the mouse spleen. Using mathematical modeling, we analyze recent data on the loss of target cells pulsed with three different peptides from the mouse lymphocytic choriomeningitis virus (LCMV) in mouse spleens with varying numbers of epitope-specific CD8 T cells. We find that the killing of targets follows the law of mass-action, i.e., the death rate of individual target cells remains proportional to the frequency (or the total number) of specific CD8 T cells in the spleen despite the fact that effector cell densities and effector to target ratios vary about a 1000-fold. The killing rate of LCMV-specific CD8 T cells is largely independent of T cell specificity and differentiation stage. Our results thus allow one to calculate the critical T cell concentration at which growth of a virus with a given replication rate can be prevented from the start of infection by memory CD8 T cell response

T Cell-Dependence of Lassa Fever Pathogenesis

Lassa virus (LASV), the causative agent of Lassa fever (LF), is endemic in West Africa, accounting for substantial morbidity and mortality. In spite of ongoing research efforts, LF pathogenesis and mechanisms of LASV immune control remain poorly understood. While normal laboratory mice are resistant to LASV, we report that mice expressing humanized instead of murine MHC class I (MHC-I) failed to control LASV infection and develop severe LF. Infection of MHC-I knockout mice confirmed a key role for MHC-I-restricted T cell responses in controlling LASV. Intriguingly we found that T cell depletion in LASV-infected HHD mice prevented disease, irrespective of high-level viremia. Widespread activation of monocyte/macrophage lineage cells, manifest through inducible NO synthase expression, and elevated IL-12p40 serum levels indicated a systemic inflammatory condition. The absence of extensive monocyte/macrophage activation in T cell-depleted mice suggested that T cell responses contribute to deleterious innate inflammatory reactions and LF pathogenesis. Our observations in mice indicate a dual role for T cells, not only protecting from LASV, but also enhancing LF pathogenesis. The possibility of T cell-driven enhancement and immunopathogenesis should be given consideration in future LF vaccine development

Repetitive Immunization Enhances the Susceptibility of Mice to Peripherally Administered Prions

The susceptibility of humans and animals to prion infections is determined by the virulence of the infectious agent, by genetic modifiers, and by hitherto unknown host and environmental risk factors. While little is known about the latter two, the activation state of the immune system was surmised to influence prion susceptibility. Here we administered prions to mice that were repeatedly immunized by two initial injections of CpG oligodeoxynucleotides followed by repeated injections of bovine serum albumin/alum. Immunization greatly reduced the required dosage of peripherally administered prion inoculum necessary to induce scrapie in 50% of mice. No difference in susceptibility was observed following intracerebral prion challenge. Due to its profound impact onto scrapie susceptibility, the host immune status may determine disease penetrance after low-dose prion exposure, including those that may give rise to iatrogenic and variant Creutzfeldt-Jakob disease