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Following a proposal made by the French and German Ministers for Foreign Affairs at the November 2020 Paris Peace Forum, 4 global partners, the Food and Agriculture Organization (FAO), the World Organization for Animal Health (OIE), the United Nations Environment Programme (UNEP), and the World Health Organization (WHO), in May 2021 established the interdisciplinary One Health High-Level Expert Panel (OHHLEP) (https://www.who.int/groups/one-health-high-level-expert-panel) to enhance their cross-sectoral collaboration. There is no shortage of “One Health” definitions in the published literature and among institutions and organizations. [...]an immediate priority for OHHLEP was to develop consensus around a working definition as a solid basis to support a common understanding among the panel members and the partner organizations. Key underlying principles including 1. equity between sectors and disciplines; 2. sociopolitical and multicultural parity (the doctrine that all people are equal and deserve equal rights and opportunities) and inclusion and engagement of communities and marginalized voices; 3. socioecological equilibrium that seeks a harmonious balance between human–animal–environment interaction and acknowledging the importance of biodiversity, access to sufficient natural space and resources, and the intrinsic value of all living things within the ecosystem; 4. stewardship and the responsibility of humans to change behavior and adopt sustainable solutions that recognize the importance of animal welfare and the integrity of the whole ecosystem, thus securing the well-being of current and future generations; and 5. transdisciplinarity and multisectoral collaboration, which includes all relevant disciplines, both modern and traditional forms of knowledge and a broad representative array of perspectives. PLoS Pathog 18(6): e1010537. https://doi.org/10.1371/journal.ppat.1010537 About the Authors: One Health High-Level Expert Panel (OHHLEP) Wiku B. Adisasmito Affiliation: Universitas Indonesia, Depok, West Java, Indonesia Salama Almuhairi Affiliation: National Emergency Crisis and Disasters Management Authority, Abu Dhabi, United Arab Emirates Casey Barton Behravesh Affiliation: Centers for Disease Control and Prevention, Atlanta, Georgia, United States of America Pépé Bilivogui Affiliation: World Health Organization, Guinea Country Office, Conakry, Guinea Salome A. Bukachi Affiliation: Institute of Anthropology, Gender and African Studies, University of Nairobi, Nairobi, Kenya Natalia Casas Affiliation: National Ministry of Health, Autonomous City of Buenos Aires, Argentina Natalia Cediel Becerra Affiliation: School of Agricultural Sciences, Universidad de La Salle, Bogotá, Colombia Dominique F. Charron Affiliation: International Development Research Centre, Ottawa, Canada Abhishek Chaudhary Affiliation: Indian Institute of Technology (IIT), Kanpur, India Janice R. Ciacci Zanella Affiliation: Brazilian Agricultural Research Corporation (Embrapa), Embrapa Swine and Poultry, Concórdia, Santa Catarina, Brazil Andrew A. Cunningham Affiliation: Institute of Zoology, Zoological Society of London, London, United Kingdom Osman Dar Affiliations Global Operations Division, United Kingdom Health Security Agency, London, United Kingdom, Global Health Programme, Chatham House, Royal Institute of International Affairs, London, United Kingdom Nitish Debnath Affiliation: Fleming Fund Country Grant to Bangladesh, DAI Global, Dhaka, Bangladesh Baptiste Dungu Affiliations Afrivet B M, Pretoria, South Africa, Faculty of Veterinary Science, University of Kinshasa, Kinshasa, Democratic Republic Congo Elmoubasher Farag Affiliation: Ministry of Public Health, Health Protection & Communicable Diseases Division, Doha, Qatar George F. Gao Affiliation: Chinese Center for Disease Control and Prevention, Beijing, People’s Republic of China David T. S. Hayman Affiliation: Molecular Epidemiology and Public Health Laboratory, Massey University, Palmerston North, New Zealand Margaret Khaitsa Affiliation: Mississippi State University, Starkville, Mississippi,

Rejection of allografts has always been the major obstacle to transplantation success. We aimed to improve characterisation of different kidney-allograft rejection phenotypes, identify how each one is associated with anti-HLA antibodies, and investigate their distinct prognoses. Patients who underwent ABO-compatible kidney transplantations in Necker Hospital and Saint-Louis Hospital (Paris, France) between Jan 1, 1998, and Dec 31, 2008, were included in our population-based study. We assessed patients who provided biopsy samples for acute allograft rejection, which was defined as the association of deterioration in function and histopathological lesions. The main outcome was kidney allograft loss—ie, return to dialysis. To investigate distinct rejection patterns, we retrospectively assessed rejection episodes with review of graft histology, C4d in allograft biopsies, and donor-specific anti-HLA antibodies. 2079 patients were included in the main analyses, of whom 302 (15%) had acute biopsy-proven rejection. We identified four distinct patterns of kidney allograft rejection: T cell-mediated vascular rejection (26 patients [9%]), antibody-mediated vascular rejection (64 [21%]), T cell-mediated rejection without vasculitis (139 [46%]), and antibody-mediated rejection without vasculitis (73 [24%]). Risk of graft loss was 9·07 times (95 CI 3·62–19·7) higher in antibody-mediated vascular rejection than in T cell-mediated rejection without vasculitis (p<0·0001), compared with an increase of 2·93 times (1·1–7·9; P=0·0237) in antibody-mediated rejection without vasculitis and no significant rise in T cell-mediated vascular rejection (hazard ratio [HR] 1·5, 95% CI 0·33–7·6; p=0·60). We have identified a type of kidney rejection not presently included in classifications: antibody-mediated vascular rejection. Recognition of this distinct phenotype could lead to the development of new treatment strategies that could salvage many kidney allografts. None.

Changes in the epidemiology and ecology of H5N1 highly pathogenic avian influenza are devastating wild bird and poultry populations, farms and communities, and wild mammals worldwide. Having originated in farmed poultry, H5N1 viruses are now spread globally by wild birds, with transmission to many mammal and avian species, resulting in 2024 in transmission among dairy cattle with associated human cases. These ecological changes pose challenges to mitigating the impacts of H5N1 highly pathogenic avian influenza on wildlife, ecosystems, domestic animals, food security, and humans. H5N1 highly pathogenic avian influenza highlights the need for One Health approaches to pandemic prevention and preparedness, emphasising multisectoral collaborations among animal, environmental, and public health sectors. Action is needed to reduce future pandemic risks by preventing transmission of highly pathogenic avian influenza among domestic and wild animals and people, focusing on upstream drivers of outbreaks, and ensuring rapid responses and risk assessments for zoonotic outbreaks. Political commitment and sustainable funding are crucial to implementing and maintaining prevention programmes, surveillance, and outbreak responses.

Within this perspective, R. Dressel and W.H. Zimmermann group proposed MHC-haploidentical parthenogenetic stem cells derived by pharmacological activation of unfertilized oocytes, as an alternative PSC-type allogenic source of therapeutic cells with less immunogenetic complexity. [...]the current state-of-the-art might forecast the application of allogeneic stem cells followed by their cell-free extracellular vesicles/exosomes as a strategy that will not only elicit the cell-contact mediated reparative/regenerative immune response but also have the desired long-lasting effects through their generated products. Conflict of Interest Statement The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. 1.OchandoJCharronDBaptistaPMUygunBE.Immune responses to bioengineered organs.Curr Opin Organ Transplant.

Organ transplantation represents a unique therapeutic option for irreparable organ dysfunction and rejection of transplants results from a breakdown in operational tolerance. Although endothelial cells (ECs) are the first target in graft rejection following kidney transplantation, their capacity to alloactivate and generate particular T lymphocyte subsets that could intervene in this process remains unknown. By using an experimental model of microvascular endothelium, we demonstrate that, under inflammatory conditions, human ECs induced proliferation of memory CD4⁺CD45RA⁻ T cells and selectively amplified proinflammatory Th17 and suppressive CD45RA⁻HLA-DR⁺FoxP3bright regulatory CD4⁺ T lymphocytes (Tregs). Although HLA-DR expression on resting microvascular ECs was sufficient to induce proliferation of memory CD4⁺ T cells, Treg amplification was dependent on the interaction with CD54, highly expressed only under inflammatory conditions. Moreover, expansion of Th17 cells was dependent on IL-6 and STAT-3, and inhibition of either specifically impaired Th17, without altering Treg expansion. Collectively these data reveal that the HLA-DR⁺ ECs regulate the local inflammatory allogeneic response, promoting either an IL-6/STAT-3-dependent Th17 response or a contact-CD54-dependent regulatory response according to the cytokine environment. Finally, these data open therapeutic perspectives in human organ transplantation based on targeting the IL-6/STAT-3 pathway and/or promoting CD54 dependent Treg proliferation.

To perform a post-outbreak prospective study of the Pseudomonas aeruginosa contamination at the faucets (water, aerator and drain) by culture and quantitative polymerase chain reaction (qPCR) and to assess environmental factors influencing occurrence A 450-bed pediatric university hospital in Montreal, Canada Water, aerator swab, and drain swab samples were collected from faucets and analyzed by culture and qPCR for the post-outbreak investigation. Water microbial and physicochemical parameters were measured, and a detailed characterization of the sink environmental and design parameters was performed. The outbreak genotyping investigation identified drains and aerators as the source of infection. The implementation of corrective measures was effective, but post-outbreak sampling using qPCR revealed 50% positivity for P. aeruginosa remaining in the water compared with 7% by culture. P. aeruginosa was recovered in the water, the aerator, and the drain in 21% of sinks. Drain alignment vs the faucet and water microbial quality were significant factors associated with water positivity, whereas P. aeruginosa load in the water was an average of 2 log higher for faucets with a positive aerator. P. aeruginosa contamination in various components of sink environments was still detected several years after the resolution of an outbreak in a pediatric university hospital. Although contamination is often not detectable in water samples by culture, P. aeruginosa is present and can recover its culturability under favorable conditions. The importance of having clear maintenance protocols for water systems, including the drainage components, is highlighted.

To investigate the association between severity of acute kidney injury (AKI) and outcome, systemic inflammatory phenotype and HLA genotype in severe sepsis. Prospective multicenter observational study done in 4 intensive care units in two university hospitals. Severe sepsis and septic shock patients with at least 2 organ failures based on the SOFA score were classified: 1) \"no AKI\", 2) \"mild AKI\" (grouping stage 1 and 2 of AKIN score) and 3) \"severe AKI\" (stage 3 of AKIN score). Sequential measurements: The vasopressor dependency index (VDI; dose and types of drugs) to evaluate the association between hemodynamic status and the development of early AKI; plasma levels of IL-10, macrophage migration inhibitory factor (MIF), IL-6 and HLA-DR monocyte expression. Genotyping of the 13 HLA-DRB1 alleles with deduction of presence of HLA-DRB3, -DRB4 and -DRB5 genes. We used multivariate analysis with competitive risk model to study associations. Overall, 176 study patients (146 with septic shock) were classified from AKIN score as \"no AKI\" (n = 43), \"mild AKI\" (n = 74) or \"severe AKI\" (n = 59). The VDI did not differ between groups of AKI. After adjustment, \"mild and severe AKI\" were an independent risk factor for mortality (HR 2.42 95%CI[1.01-5.83], p = 0.048 and HR 1.99 95%CI[1.30-3.03], p = 0.001 respectively). \"Severe AKI\" had higher levels of plasma IL-10, MIF and IL-6 compared to \"no AKI\" and mild AKI (p<0.05 for each), with no difference in mHLA-DR at day 0. HLA-DRB genotyping showed a significantly lower proportion of 4 HLA-DRB alleles among patients requiring renal replacement therapy (RRT) (58%) than in patients with severe AKI who did not receive RRT (84%) (p = 0.004). AKI severity is independently associated with mortality and plasma IL-10, MIF or IL-6 levels. Presence of 4 alleles of HLA-DRB in severe AKI patients seems associated with a lower need of RRT.

Background Enteric diseases affect thousands of Canadians annually and several large outbreaks have occurred due to infection with enteric pathogens. The objectives of this study were to describe the spatial and temporal distributions of reportable Campylobacter , Escherichia coli , Giardia , Salmonella and Shigella from 1994 to 2002 in New Brunswick, Canada. By examining the spatial and temporal distributions of disease incidence, hypotheses as to potential disease risk factors were formulated. Methods Time series plots of monthly disease incidence were examined for seasonal and secular trends. Seasonality of disease incidence was evaluated using the temporal scan statistic and seasonal–trend loess (STL) decomposition methods. Secular trends were evaluated using negative binomial regression modeling. The spatial distribution of disease incidence was examined using maps of empirical Bayes smoothed estimates of disease incidence. Spatial clustering was examined by multiple methods, which included Moran’s I and the spatial scan statistic. Results The peak incidence of Giardia infections occurred in the spring months. Salmonella incidence exhibited two peaks, one small peak in the spring and a main peak in the summer. Campylobacter and Escherichia coli O157 disease incidence peaked in the summer months. Moran’s I indicated that there was significant positive spatial autocorrelation for the incidence of Campylobacter , Giardia and Salmonella . The spatial scan statistic identified clusters of high disease incidence in the northern areas of the province for Campylobacter , Giardia and Salmonella infections. The incidence of Escherichia coli infections clustered in the south-east and north-east areas of the province, based on the spatial scan statistic results. Shigella infections had the lowest incidence rate and no discernable spatial or temporal patterns were observed. Conclusions By using several different spatial and temporal methods a robust picture of the spatial and temporal distributions of enteric disease in New Brunswick was produced. Disease incidence for several reportable enteric pathogens displayed significant geographic clustering indicating that a spatially distributed risk factor may be contributing to disease incidence. Temporal analysis indicated peaks in disease incidence, including previously un-reported peaks.

Gene-environment interactions may play an important role in modulating the impact of early-life stressful events on the clinical course of bipolar disorder (BD), particularly associated to early age at onset. Immune dysfunction is thought to be an important mechanism linking childhood trauma with early-onset BD, thus the genetic diversity of immune-related loci may account for an important part of the interindividual susceptibility to this severe subform. Here we investigated the potential interaction between genetic variants of Toll-like receptors 2 (TLR2) and 4 (TLR4), major innate immune response molecules to pathogens, and the childhood trauma questionnaire (CTQ) in age at onset of BD. We recruited 531 BD patients (type I and II or not otherwise specified), genotyped for the TLR2 rs4696480 and rs3804099 and TLR4 rs1927914 and rs11536891 single-nucleotide polymorphisms and recorded for history of childhood trauma using the CTQ. TLR2 and TLR4 risk genotype carrier state and history of childhood emotional, physical and sexual abuses were evaluated in relation to age at onset as defined by the age at first manic or depressive episode. We observed a combined effect of TLR2 rs3804099 TT genotype and reported sexual abuse on determining an earlier age at onset of BD by means of a Kaplan-Meier survival curve (p = 0.002; corrected p = 0.02). Regression analysis, however, was non-significant for the TLR2-CTQ sexual abuse interaction term. The negative effects of childhood sexual abuse on age at onset of BD may be amplified in TLR2 rs3804099 risk genotype carriers through immune-mediated pathways. Clinical characteristics of illness severity, immune phenotypes and history of early life infectious insults should be included in future studies involving large patient cohorts.