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Hypoglycin A and methylenecyclopropylglycine are protoxins responsible for atypical myopathy in equids. These protoxins are converted into toxins that inhibit fatty acid β-oxidation, leading to blood accumulation of acylcarnitines and toxin conjugates, such as methylenecyclopropylacetyl-carnitine. The enzymes involved in this activation are also present in some prokaryotic cells, raising questions about the potential role of intestinal microbiota in the development of intoxication. Differences have been noted between the faecal microbiota of cograzers and atypical myopathy-affected horses. However, recent blood acylcarnitines profiling revealed subclinical cases among cograzers, challenging their status as a control group. This study investigates the faecal microbiota of horses clinically affected by atypical myopathy, their cograzers, and a control group of toxin-free horses while analysing correlations between microbiota composition and blood parameters. Faecal samples were analysed using 16S amplicon sequencing, revealing significant differences in α-diversity, evenness, and β-diversity. Notable differences were found between several genera, especially Clostridia_ge, Bacteria_ge, Firmicutes_ge, Fibrobacter, and NK4A214_group. Blood levels of methylenecyclopropylacetyl-carnitine and C14:1 correlated with variations in faecal microbial composition. The theoretical presence of enzymes in bacterial populations was also investigated. These results underscore the critical need to investigate the potential role of intestinal microbiota in this poisoning and may provide insights for developing prevention and treatment strategies.

Hypoglycin A is a plant-derived protoxin that causes atypical myopathy in equids. In atypical myopathy-affected horses, metabolomic and microbiome studies have reported alterations in metabolic markers and faecal microbiota composition, pointing to a potential disruption of microbial homeostasis. However, in vivo observations are strongly confounded by host-related factors, underscoring the need for controlled in vitro approaches. To address this, we used an in vitro static batch fermentation model simulating the equine colon to investigate the direct effects of hypoglycin A on microbiota composition and activity. Faecal inocula from healthy horses were incubated in control and hypoglycin A-treated fermenters for 48 h, with serial analyses of hypoglycin A concentration, short-chain fatty acids, and 16S rRNA gene profiles. Hypoglycin A remained stable in the nutritive medium in the absence of microbiota, confirming that its degradation in inoculated fermenters was microbiota-dependent. The results showed significant microbial-associated hypoglycin A degradation without evidence of toxic metabolite formation. The analysis of α- and β-diversity revealed both an effect of incubation time, reflecting the natural temporal dynamics of microbial communities under batch fermentation, and a specific impact of hypoglycin A exposure, with certain taxa such as Paraclostridium being affected. This study provides the first in vitro evidence that the equine microbiota contributes to hypoglycin A degradation.

Le microbiote intestinal est un terme désignant l’ensemble des micro-organismes présents dans la lumière digestive. Depuis quelques années, son étude connaît un essor considérable grâce au développement de la génomique. Les maladies inflammatoires chroniques de l’intestin (MICI), la maladie de Crohn et la rectocolite hémorragique sont des pathologies apparues au fur et à mesure de l’occidentalisation du mode de vie. Le microbiote intestinal étant un acteur majeur de la physiologie intestinale et sensible aux modifications environnementales, l’hypothèse d’un rôle pivot du microbiote intestinal dans la pathogénie des MICI s’est donc imposée. Le microbiote intestinal des patients atteints d’une MICI se caractérise par des différences de composition et d’activité métabolique par rapport aux sujets sains. Une dysbiose, c’est-à-dire un déséquilibre entre les bactéries pro-inflammatoires et anti-inflammatoires, est observée, associée à une perte de la diversité et à une activité fonctionnelle modifiée. Néanmoins, le rôle causal du microbiote dans la pathogénie des MICI n’est pas clairement élucidé. Pour l’instant, cette analyse du microbiote n’a pas d’intérêt en pratique clinique à l’échelon individuel. Néanmoins, dans les années à venir, il pourrait servir de biomarqueur pour prédire l’évolution de la maladie ou la réponse au traitement. Les applications thérapeutiques sont encore au stade de l’essai clinique mais que ce soit via l’alimentation ou la transplantation de microbiote fécal, des prises en charge ayant comme cible le microbiote devraient voir le jour dans les prochaines années pour les patients atteints d’une MICI. Intestinal microbiota is defined as the community of microorganisms present in the gut lumen. Recent advances in genomics made enhanced microbiota knowledge possible. Inflammatory Bowel Diseases (IBD) were first observed in industrialized countries. Gut microbiota, critical determinant of intestinal physiology and susceptible to environment modifications, is suspected to play a key role in their pathophysiology. Gut microbiota from IBD patients display composition and functional differences compared to healthy subjects. A dysbiosis, namely an imbalance between pro- and anti-inflammatory bacteria is observed, next to a loss of diversity and modified metabolic activity. However, the role of microbiota in IBD has not been thoroughly elucidated yet. Currently, microbiota analysis is not indicated in routine practice and presents no interest at the individual scale. Hopefully, in the coming years, microbiota could be used as a biomarker to predict disease outcomes or response to therapy. Therapeutic applications are being tested in many clinical trials but have not yet been translated in the clinical practice. However, therapeutic management taking microbiota as a target could be soon integrated in clinical practice, through specific diets or fecal microbiota transplantation.

La transplantation de microbiote fécal (TMF) est actuellement indiquée en France dans le traitement des infections à Clostridium difficile à partir de la deuxième récidive. Son recueil, sa préparation et son administration obéissent à un protocole standardisé. Son indication pourrait être élargie à de nombreuses autres disciplines médicales durant les prochaines années. Fecal microbiota transplantation (FMT) is indicated as a treatment for Clostridium difficile infections from the second recurrence. Its collection, preparation and administration follow a well-defined protocol. It could be used in the coming years in many other medical disciplines.

La pérdida del control de la ingesta alimentaria es un factor crucial en el desarrollo de la obesidad. Una alteración cognitiva importante asociada con la pérdida del control de la ingesta alimentaria y la obesidad es el deterioro de la flexibilidad cognitiva y el control inhibitorio. Un número cada vez mayor de estudios confirman que la microbiota intestinal contribuye significativamente a la pérdida del control de la ingesta alimentaria, la obesidad y la función cognitiva. En base a estos datos, hemos investigado si la transferencia de microbiota intestinal de humanos con obesidad/ normopeso y flexibilidad cognitiva deteriorada/no deteriorada podría afectar sustancialmente esta respuesta conductual en ratones expuestos a una dieta obesogénica frente a una dieta estándar. Los ratones fueron tratados previamente con un cóctel de antibióticos y luego recibieron un trasplante de microbiota intestinal de humanos. Posteriormente, se realizaron diferentes test de comportamiento para evaluar la flexibilidad cognitiva como una medida del control inhibitorio. El tratamiento con antibióticos deterioró significativamente la memoria a corto plazo en ratones, como se ha informado previamente. Es importante destacar que los ratones que recibieron microbiota de sujetos con alta y baja flexibilidad cognitiva modificaron su rendimiento de memoria a corto y largo plazo en función de la exposición a la dieta. En resumen, este estudio muestra que la microbiota intestinal es un factor que contribuye de manera importante a la flexibilidad cognitiva, lo que puede abrir nuevas estrategias terapéuticas para combatir la pérdida de control de la ingesta alimentaria y las comorbilidades metabólicas asociadas. Palabras clave: Adicción a la comida, obesidad, microbiota intestinal, deterioro cognitivo, trasplante de microbiota fecal Loss of eating control is a crucial factor in developing obesity, which has become a global health concern, causing important cardiovascular, metabolic, emotional, and cognitive co-morbidities. A major cognitive alteration associated with loss of eating control and obesity is the impairment of cognitive flexibility and inhibitory control. An increasing number of studies confirm that gut microbiota is a significant contributor to loss of eating control, obesity, and cognitive function. Therefore, we have investigated whether gut microbiota transfer from humans with impaired/ not impaired cognitive flexibility could substantially affect this behavioral response in mice in the context of obesogenic versus standard diet. Mice were pretreated with an antibiotic cocktail and later received a gut microbiota transplant from human subjects. The transferred microbiota was maintained in mice for seven weeks. Afterward, behavioral tests were performed to evaluate different cognitive responses, locomotor activity, anxiety-like, and depression-like behaviors. Antibiotic treatment significantly impaired short-term memory in mice, as previously reported. Furthermore, mice that received microbiota from high and low cognitive flexibility subjects modified their short-term and long-term memory performance depending on the diet exposure. Slight changes were observed in the locomotor activity, primarily in the high-fat diet-fed antibiotic-treated mice, and no significant alterations were observed in anxiety-like or depressive-like behaviors. In summary, this study shows that gut microbiota is a major contributor to cognitive flexibility, which may open novel therapeutic strategies for combating loss of eating control and related metabolic co-morbidities. Keywords: Loss of eating control, obesity, food addiction, gut microbiota, cognitive flexibility, fecal microbiota transplant

Equine atypical myopathy (AM) is caused by hypoglycin A (HGA) and methylenecyclopropylglycine (MCPG) intoxication resulting from the ingestion of seeds or seedlings of some Acer tree species. Interestingly, not all horses pasturing in the same toxic environment develop signs of the disease. In other species, it has been shown that the intestinal microbiota has an impact on digestion, metabolism, immune stimulation and protection from disease. The objective of this study was to characterize and compare fecal microbiota of horses suffering from AM and healthy co-grazers. Furthermore, potential differences in fecal microbiota regarding the outcome of diseased animals were assessed. This prospective observational study included 59 horses with AM (29 survivors and 30 non-survivors) referred to three Belgian equine hospitals and 26 clinically healthy co-grazers simultaneously sharing contaminated pastures during spring and autumn outbreak periods. Fresh fecal samples (rectal or within 30 min of defecation) were obtained from all horses and bacterial taxonomy profiling obtained by 16S amplicon sequencing was used to identify differentially distributed bacterial taxa between AM-affected horses and healthy co-grazers. Fecal microbial diversity and evenness were significantly (p < 0.001) higher in AM-affected horses as compared with their non-affected co-grazers. The relative abundance of families Ruminococcaceae, Christensenellaceae and Akkermansiaceae were higher (p ≤ 0.001) whereas those of the Lachnospiraceae (p = 0.0053), Bacteroidales (p < 0.0001) and Clostridiales (p = 0.0402) were lower in horses with AM, especially in those with a poor prognosis. While significant shifts were observed, it is still unclear whether they result from the disease or might be involved in the onset of disease pathogenesis.

Negli ultimi anni, il microbiota intestinale è stato oggetto di innumerevoli studi condotti sia su modelli murini sia su popolazione umana al fine di valutare funzioni e interazioni con l’ospite, quali nutrizione, omeostasi metabolica, protezione dalle infezioni e sviluppo dell’immunità sistemica e mucosale nelle malattie infiammatorie croniche intestinali (MICI) così come in altre malattie intestinali ed extraintestinali. Nelle MICI il microbiota intestinale appare alterato in composizione, biodiversità, stabilità e funzioni. Anche la riduzione di F. prausnitzii, l’aumento di Proteonbacteria così come l’aumento di Candida albicans, del ratio Basidiomycota/Ascomycota su Saccharomyces cerevisiae e Caudovirales sopra Microviridae, sono tutte caratteristiche tipiche della disbiosi osservata nelle MICI. La modulazione indiretta (mediante antibiotici, probiotici) e diretta (mediante fecal microbiota transplantation) del gut microbiota ha implicazioni cliniche rilevanti nel management delle MICI. Il prossimo futuro chiarirà il ruolo e l’implicazione clinica della caratterizzazione del gut microbiota nell’approccio personalizzato della terapia delle IBD.

Le syndrome de l’intestin irritable (SII) est une maladie complexe composée de sous-groupes hétérogènes de patients. Les traitements actuels ne sont pas satisfaisants quant à leur efficacité. Le microbiote intestinal, objet d’études de plus en plus nombreuses, est potentiellement impliqué dans la physiopathologie du SII. Il n’existe pas de signature microbienne particulière de la maladie, mais certaines caractéristiques du microbiote sont associées à sa sévérité. Certains traitements modifiant entre autres effets la composition du microbiote intestinal ont prouvé leur efficacité dans cette pathologie, comme les probiotiques, les modifications de l’alimentation, certains antibiotiques non absorbables et plus récemment la transplantation fécale. De nouvelles perspectives thérapeutiques s’ouvrent avec l’avancée des technologies offrant de nouveaux moyens de moduler la composition du microbiote intestinal. Une caractérisation précise de cette composition, en prenant en compte les nombreux biais liés aux méthodes d’analyse et les sousgroupes symptomatiques de patients, permettra sans doute à terme de proposer des traitements personnalisés efficaces. Irritable bowel syndrome is a complex disease made up of heterogeneous subgroups of patients. Current treatments are not satisfactory in terms of their effectiveness. The gut microbiota, subject of an increasing number of studies, is potentially involved in the pathophysiology of irritable bowel syndrome. There is no specific microbial signature of the disease, but certain characteristics of the microbiota are associated with its severity. Certain treatments modifying, among other effects, the composition of the intestinal microbiota have proven their effectiveness in this pathology, such as probiotics, changes in diet, certain non-absorbable antibiotics, and more recently fecal transplantation. New therapeutic perspectives are opening with the advancement of technologies offering new means of modulating the composition of the intestinal microbiota. A precise characterization of this composition, considering the many biases that are linked to the analysis methods and the symptomatic subgroups of patients, will ultimately allow us to offer effective personalized treatments to patients.

Un desequilibrio en la microbiota intestinal (MI) influye en el desarrollo de la obesidad. Una estrategia para tratar la obesidad implicaría restaurar el equilibrio, manipulando la MI. La efectividad del trasplante fecal (TF) en ciertas patologías, la respalda como una terapia alternativa. La comunidad de indios Pima (PI) son referente en el estudio de la etiología de la diabetes mellitus tipo 2 y obesidad. Se analizó el TF como estrategia preventiva en el desarrollo de obesidad en PI. Para ello, se recogieron evidencias científicas mediante una revisión sistemática cualitativa desde el año 2000 al 2013. Los resultados mostraron un aumento del 112% en el número de publicaciones científicas que asocian la salud a la MI. Un 13% de los estudios relacionan una asociación de la MI con la obesidad. No se encontró ningún estudio de la composición de la MI en los PI. Respecto al TF, se encontró que es el tratamiento menos utilizado para restaurar la microbiota. Se concluyó que, existe un creciente interés científico en el estudio de la MI y se evidenciaron dos brechas de investigación: composición de la MI en los PI y estudios acerca del TF, para determinar su efectividad como terapia preventiva de la obesidad.