Impact of pleasure-oriented messages on food choices : is it more effective than traditional health-oriented messages to promote healthy eating ?

Some authors have suggested that eating pleasure is underused to promote healthy eating. However, little is known about the potential of pleasure-oriented messages to lead to healthier food choices. The aim of this study was to examine the effects of pleasure- and health-oriented messages on food choices made from a buffet. One hundred and ninety-eight participants (50% women), unaware of the real objective of the study, were randomized in three groups: 1) pleasure, 2) health, and 3) control. They first completed three 24h food recalls to assess their overall diet quality using the Canadian Healthy Eating Index (C-HEI; score: 0 to 100). Thereafter, participants came to the research institute and those randomized in the “pleasure” and “health” groups read a leaflet on healthy eating, using either a pleasure or a health orientation respectively. Participants in the control group had no leaflet to read. All participants had subsequently to choose four food items in a buffet offering both healthy and unhealthy foods. Results showed a group by diet quality interaction (p=0.02). Among participants with lower diet quality (C-HEI score below 50), those in the pleasure and health groups were more likely than participants in the control group to choose a healthier main course (prevalence ratios (PR) 1.71, 95% CI 1.12-2.62 and 1.83, 95% CI 1.21-2.77 for the pleasure and health group respectively) and a healthier beverage (PR 1.67, 95% CI 1.02-2.71 and 1.66, 95% CI 1.02-2.72, respectively). No such effect was observed among participants with higher C-HEI scores. In conclusion, our results suggest that in people with sub-optimal dietary habits, pleasure-oriented messages and traditional health messages are both useful to favor healthy main course and beverage choices

UM171 induces a homeostatic inflammatory-detoxification response supporting human HSC self-renewal.

Elucidation of the molecular cues required to balance adult stem cell self-renewal and differentiation is critical for advancing cellular therapies. Herein, we report that the hematopoietic stem cell (HSC) self-renewal agonist UM171 triggers a balanced pro- and anti-inflammatory/detoxification network that relies on NFKB activation and protein C receptor-dependent ROS detoxification, respectively. We demonstrate that within this network, EPCR serves as a critical protective component as its deletion hypersensitizes primitive hematopoietic cells to pro-inflammatory signals and ROS accumulation resulting in compromised stem cell function. Conversely, abrogation of the pro-inflammatory activity of UM171 through treatment with dexamethasone, cAMP elevating agents or NFkB inhibitors abolishes EPCR upregulation and HSC expansion. Together, these results show that UM171 stimulates ex vivo HSC expansion by establishing a critical balance between key pro- and anti-inflammatory mediators of self-renewal

Nucleocapsid-specific and PD-L1+CXCR3+ CD8 polyfunctional T-cell abundances are associated with survival of critical SARS-CoV2-infected patients

International audienceRationale. The importance of the adaptative T cell response in the control and resolution of viral infection has been well-established. However, the nature of T cell-mediated viral control mechanisms in life-threatening stages of COVID-19 has yet to be determined.Objective. The aim of the present study was to determine the function and phenotype of T cell populations associated with survival or death of COVID-19 patients under intensive care as a result of phenotypic and functional profiling by mass cytometry.Findings. Increased frequencies of circulating, polyfunctional, CD4+CXCR5+HLA-DR+ stem cell memory T cells (TSCM) and decreased proportions of Granzyme-B and Perforin-expressing effector memory T cells (TEM) were detected in recovered and deceased patients, respectively. The higher abundance of polyfunctional CD8+PD-L1+CXCR3+ T effector cells, CXCR5+HLA-DR+ TSCM, as well as anti-nucleocapsid (NC) cytokine-producing T cells permitted to differentiate between recovered and deceased patients. The results from a principal component analysis showed an imbalance in the T cell compartment allowed for the separation of recovered and deceased patients. The paucity of circulating CD8+PD-L1+CXCR3+ Teff-cells and NC-specific CD8+ T-cells accurately forecasts fatal disease outcome.Conclusion. This study provides insight into the nature of the T cell populations involved in the control of COVID-19 and therefor might impact T cell-based vaccine designs for this infectious disease

NBEAL2 deficiency in humans leads to low CTLA-4 expression in activated conventional T cells

Abstract Loss of NBEAL2 function leads to grey platelet syndrome (GPS), a bleeding disorder characterized by macro-thrombocytopenia and α-granule-deficient platelets. A proportion of patients with GPS develop autoimmunity through an unknown mechanism, which might be related to the proteins NBEAL2 interacts with, specifically in immune cells. Here we show a comprehensive interactome of NBEAL2 in primary T cells, based on mass spectrometry identification of altogether 74 protein association partners. These include LRBA, a member of the same BEACH domain family as NBEAL2, recessive mutations of which cause autoimmunity and lymphocytic infiltration through defective CTLA-4 trafficking. Investigating the potential association between NBEAL2 and CTLA-4 signalling suggested by the mass spectrometry results, we confirm by co-immunoprecipitation that CTLA-4 and NBEAL2 interact with each other. Interestingly, NBEAL2 deficiency leads to low CTLA-4 expression in patient-derived effector T cells, while their regulatory T cells appear unaffected. Knocking-down NBEAL2 in healthy primary T cells recapitulates the low CTLA-4 expression observed in the T cells of GPS patients. Our results thus show that NBEAL2 is involved in the regulation of CTLA-4 expression in conventional T cells and provide a rationale for considering CTLA-4-immunoglobulin therapy in patients with GPS and autoimmune disease