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Inflammatory bowel disease (IBD), which includes ulcerative colitis and Crohn's disease, is thought to develop in genetically predisposed individuals as a consequence of complex interactions between dysregulated inflammatory stimuli, immunological responses, and environmental factors. The pathogenesis of IBD has yet to be fully understood. The global increase in the incidence of IBD suggests a gap in the current understanding of the disease. The development of a new diagnostic tool for inflammatory bowel disease that is both less invasive and more cost-effective would allow for better management of this condition. MicroRNAs (miRNAs) are a class of noncoding RNAs with important roles as posttranscriptional regulators of gene expression, which has led to new insights into understanding IBD. Using techniques such as microarrays and real-time polymerase chain reactions, researchers have investigated the patterns in which patients with Crohn's disease and ulcerative colitis show alterations in the expression of miRNA in tissue, blood, and feces. These miRNAs are found to be differentially expressed in IBD and implicated in its pathogenesis through alterations in autophagy, intestinal barrier, and immune homeostasis. In this review, we discuss the miRNA expression profiles associated with IBD in tissue, peripheral blood, and feces and provide an overview of the miRNA mechanisms involved in IBD.We review the published studies on microRNA (miRNA) expression in inflammatory bowel disease, including miRNAs extracted from blood, tissue, and stool samples. We discuss the main mechanisms of miRNA involvement in inflammatory bowel disease and their potential use as biomarkers.

International audience; Immoderate calorie intake coupled with a sedentary lifestyle are major determinants of health issues and inflammatory diseases in modern society.The balance between energy consumption and energy expenditure is critical for longevity. Excessive energy intake and adiposity cause systemicinflammation, whereas calorie restriction (CR) without malnutrition, exerts a potent anti-inflammatory effect. The objective of this review was toprovide an overview of different strategies used to reduce calorie intake, discuss physiological mechanisms by which CR might lead to improvedhealth outcomes, and summarize the present knowledge about inflammatory diseases. We discuss emerging data of observational studies andrandomized clinical trials on CR that have been shown to reduce inflammation and improve human health. Adv Nutr 2021;00:1–13.

Background Lymphoma is a dreaded complication of inflammatory bowel diseases [IBD]. Knowledge about lymphoma in patients with IBD is limited to epidemiological data and the description of risk factors. We performed a systematic review to describe the clinical characteristics and prognosis of lymphoma in patients with IBD. Methods Electronic databases were searched up to June 1, 2020. All published clinical characteristics of lymphoma occurring in patients with IBD were collected. Results Eleven studies were included. A total of 589 lymphomas were described in patients with IBD. As seen in de novo lymphoma, non-Hodgkin’s lymphoma [NHL] was the most common histological subtype [83.9%]. Diffuse large B-cell lymphoma [DLBCL] and follicular lymphoma were the most well-represented NHL in patients with IBD [30% and 13% respectively]. Two main differences were observed in comparison with de novo lymphoma: primary intestinal lymphoma [PIL] represented a large proportion of lymphoma in patients with IBD [22–75%] whereas mucosa-associated lymphoid tissue [MALT] lymphoma was under-represented. Epstein–Barr virus [EBV]-positive status was observed in a large proportion of tumours [44–75%]. Survival data of lymphoma in patients with IBD were similar to those of de novo lymphoma. Discussion This systematic review first highlights that PIL [especially DLBCL subtype] is significantly more frequent in patients with IBD and represents the most common entity. Conversely, MALT lymphoma is extremely rare in the IBD population. However, the overall quality of the evidence is low. Further studies are required to better define lymphoma characteristics in patients with IBD.

International audience; Secukinumab, ixekizumab and brodalumab are monoclonal antibody therapies that inhibit interleukin (IL)-17 activity and are widely used for the treatment of psoriasis, psoriatic arthritis and ankylosing spondylitis. The promising efficacy results in dermatology and rheumatology prompted the evaluation of these drugs in Crohn's disease and ulcerative colitis, but the onset of paradoxical events (disease exacerbation after treatment with a theoretically curative drug) prevented their approval in patients with inflammatory bowel diseases (IBDs). To date, the pathophysiological mechanisms underlying these paradoxical effects are not well defined, and there are no clear guidelines for the management of patients with disease flare or new IBD onset after anti-IL-17 drug therapy. In this review, we summarise the literature on putative mechanisms, the clinical digestive effects after therapy with IL-17 inhibitors and provide guidance for the management of these paradoxical effects in clinical practice.

International audience; Telomeres are repetitive DNA sequences located at the ends of linear chromosomes that preserve the integrity and stability of the genome. Telomere dysfunctions due to short telomeres or altered telomere structures can ultimately lead to replicative cellular senescence and chromosomal instability, both mechanisms being hallmarks of ageing. Chronic inflammation, oxidative stress and finally telomere length (TL) dynamics have been shown to be involved in various age-related non-communicable diseases (NCDs). Immune-mediated inflammatory diseases (IMIDs), including affections such as inflammatory bowel disease, psoriasis, rheumatoid arthritis, spondyloarthritis and uveitis belong to this group of age-related NCDs. Although in recent years, we have witnessed the emergence of studies in the literature linking these IMIDs to TL dynamics, the causality between these diseases and telomere attrition is still unclear and controversial. In this review, we provide an overview of available studies on telomere dynamics and discuss the utility of TL measurements in immune-mediated inflammatory diseases.

Inflammatory bowel diseases (IBD) are chronic diseases characterized by inflammation of the mucosa associated with gut microbiota dysbiosis and overreaction of the immune system. IBD prevalence is increasing in industrialized countries where the western dietary pattern is involved in many pathologies such as obesity, diabetes, and cancers. Nutrition appears to be an important environmental factor involved in IBD onset through poorly understood biological mechanisms. Here we focused on the early consequences of a diet enriched in sugar (sucrose) because it represents up to 25% of total energy intake within industrialized countries, while the WHO recommends reducing it to less than 5%. We studied the effects of high sucrose diet on intestinal homeostasis and experimental colitis in mice. In healthy subjects, this diet caused endoscopic lesions, thus predisposing to colitis. The worsening of colitis was preceded by gut microbiota dysbiosis with complete depletion of bacteria belonging to Barnesiella and transcriptional reprogramming of colonic genes, associated with IBD according to functional annotations. In cellulo, a low dose of fructose induced cell junctions’ alterations, while a high dose of glucose was needed to induce similar damage. After colitogenic treatment, the high sugar diet worsens the severity of clinical and endoscopic signs by disrupting the organization of cell-cell junctions and the autophagy process in intestinal cells. Such in-vivo effects on mice microbiome and transcriptome were partially reversible upon mice return to control diet. Finally, sugar overconsumption induces a "pre-IBD" state characterized by an overall downregulation of the colonic transcriptome in mice together with immunodepression, significant alterations in cellular architecture, and gut microbiota dysbiosis. Our findings support international recommendations about reducing sugar consumption to reduce the risk of developing or worsening intestinal inflammation., Les maladies inflammatoires chroniques de l’intestin (MICI) se caractérisent par une inflammation de la muqueuse liée à une altération du microbiote intestinal et une hyperactivité du système immunitaire. La prévalence de ces pathologies ne cesse d’augmenter dans les pays occidentaux où le régime « Western Diet » est mis en cause dans de nombreuses pathologies telles que l’obésité, le diabète ou certains cancers. La nutrition est un facteur environnement important impliqué dans les MICI par le biais de mécanismes biologiques encore mal compris. Nous nous sommes intéressés à la consommation en sucre (saccharose) car ce dernier représente jusqu’à 25 % de l’apport énergétique total dans les pays industrialisés alors que l’OMS recommande de le réduire à moins de 5 %. Nous avons étudié les effets d’un régime enrichi en saccharose sur l’homéostasie intestinale et sur la colite expérimentale chez la souris. Chez les sujets sains, ce régime a provoqué des lésions endoscopiques prédisposant ainsi les animaux à la colite. L’aggravation de la colite était précédée d’une dysbiose du microbiote intestinal, avec une déplétion totale de bactéries appartenant au genre Barnesiella et une reprogrammation transcriptionnelle des gènes coliques, associés aux MICI selon les annotations fonctionnelles. In cellulo, une faible dose de fructose a provoqué une altération des jonctions cellulaires tandis qu’une forte dose de glucose a été nécessaire pour induire des dommages similaires. Après traitement colitogène, le régime hypersucré aggrave la sévérité des signes cliniques, endoscopiques et histologiques en perturbant l’organisation des jonctions cellulaires et le processus d’autophagie dans les cellules intestinales. Les effets in vivo sur le microbiome et le transcriptome des souris se sont avérés partiellement réversibles après retour des animaux au régime contrôle. Finalement, la surconsommation de sucre a provoqué un état « pré-MICI » caractérisé par une régulation à la baisse du transcriptome colique des souris ainsi qu’une immunodépression, des altérations importantes de l’architecture cellulaire et une dysbiose du microbiote intestinal. Ainsi, nos travaux soutiennent les recommandations internationales concernant la réduction de la consommation de sucre, ce qui pourrait limiter le risque de développer et/ou d’aggraver l’inflammation intestinale.