Dr. Neeraj Narula reports a post-hoc analysis of the UNITI Crohn’s trials showing that early measurement of faecal calprotectin after induction therapy predicts clinical outcomes better than baseline measurements of calprotectin and than other week 6 clinical or biomarker data.

To provide a brief overview of the role of nutrition, diet and the dietitian in fertility, conception and pregnancy.

Educational objective:

-        To analyse Th17 plasticity in T-cell transfer colitis mouse model, and correlate this with the microbiota composition.

-        To understand whether antibiotics affect Th17 plasticity through microbiota-dependent processes.

Summary. During Inflammatory Bowel Disease (IBD), CD4+ effector T cells are main mediators of the tissue damage. Among them, Th17 cells strongly contribute to the inflammatory response. Interestingly, our lab previously showed that Th17 cells can convert into regulatory T cells, thereby controlling inflammation. However, the forces controlling the plasticity of T cells during IBD remain largely unknown. Our aim is to understand, how CD4+ T-cell plasticity can be modulated from a pro-inflammatory towards an anti-inflammatory profile during IBD. In this regard, both Th17 and Foxp3 regulatory T cells can recognize microbiota-antigens. Moreover, changes in the microbiota are commonly observed in IBD. Therefore, we hypothesize that the microbiota might be a key candidate to modulate T-cell plasticity. To address our goal, T-cell transfer mouse IBD model was performed by transferring CD4+ naïve T-cells into Rag1-/- mice. To study Th17 T-cell plasticity, we used as donors IL-17A Fate-mapping mice. Ciprofloxacin and metronidazole, antibiotics commonly given to IBD patients, were used to treat the mice. After T-cell transfer colitis induction, ciprofloxacin and metronidazole treatment ameliorated gut inflammation. In line with this, we observed a relative expansion of bacteria previously associated with beneficial IBD outcomes (e.g. Bifidobacterium). More interestingly, colon CD4+ T-cells showed an increased conversion from Th17 towards a Foxp3+ Treg profile (Foxp3ExTh17)(p=0.03).

The presentation will provide an update on the recently updated ECCO guideline on the prevention, diagnosis and management of infections in IBD

1. To understand the role of head to head trials in positioning therapies

2. To be familiar with the large pipeline of new agents for IBD including the late stage products focused on JAK inhibition, anti-p19 (interleukin 23) antibodies, and S1P modulators

3. To be familiar with the multiple agents targeting gut delivery that in early stage development

4. To be familiar with the evolving role of precision medicine and artificial intelligence in the care of IBD patients

5. To be familiar with novel clinical trial approaches are increasingly being employed in IBD including adaptive design, umbrella trials, basket trials, and platform trials

Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), are chronic, progressive, disabling condition. Since strategies targeting the control of symptoms do not significantly change the natural course of the diseases, mucosal healing has become the therapeutic goal to prevent disease recurrence and structural damage. However, frequent colonoscopies (CS) are expensive, invasive, and not well tolerated by patients, thus non-invasive tools for assessment and monitoring are strongly needed.

Bowel ultrasound (US) is a well-tolerated, non-invasive, patient friendly, cheap, easy-to-use tool to manage IBD patients in clinical practice. In addition, its ability to be performed as point-of-care bowel US may drastically change frequency of the assessment of treatment response, speeding the clinical decision-making process

This presentation aims to review the evidence for the use of bowel US, alternatively to CS, for the assessment and monitoring of disease activity in IBD.

Technical features of Entero-MRI (E-MRI) will be briefly illustrated from basic to advanced sequences.
Imaging findings of ileal Crohn’s disease will be reviewed in this talk with emphasis on their clinical meaning according to literature and Ecco/Esgar  statements.
After this talk participants of the workshop will be able to approach in a critical manner E-MRI studies and MRI structured reports giving a guide to appreciate those findings more relevant in clinical practice in patient management.
Emphasis will be given in the definition of relevant findings such as strictures, penetrating lesions, edema and fibrosis of bowel wall.
Criteria to assess inflammation activity as well as  MR scores of activity will be illustrated.
Strength and weak points  of E-MRI will be discussed

Educational objectives: 

1. To understand the risk management prior to surgery and how to prevent enterocutaneous fistulas
2. To briefly understand the pre- and peroperative management of enterocutaneous fistulas

Educational objectives:
1. To understand the rationale for FMT as a treatment for IBD.
2. To be updated on trial data for FMT in IBD.
3. To understand some emerging predictors of efficacy for FMT in IBD.
4. To understand the infrastructural needs for FMT as a therapy.
5. To understand the evolving regulatory landscape and governance issues for FMT.

Educational objectives
•What is fermentation? What are fermented food?
•History of fermented foods
•Do fermented foods necessarily contain live microorganisms?
•Are fermented foods the same as probiotic foods?
•Do microorganisms in fermented foods become established in the gut or influence gut microbiota?
•Do fermented foods provide health benefits?
• Main studies on fermented foods and gastrointestinal tract: yogurt, cheese, kefir , sourdough bread, sauerkraut, kimchi, fermented soy products

new endpoints for multiple orphan indications are being defined in this lecture

Inflammation in the Inflammatory bowel diseases may be driven by diet , as evidenced to date by the return of inflammation in patients transitioning from exclusive enteral nutrition to partial enteral nutrition. Exclusion diets such as the Crohn’s disease exclusion diets cause a decrease in inflammation and mucosal healing in Crohn’s disease. These findings suggest that certain dietary components may be one of the culprits in driving the surge of IBD around the globe. One of the key suspects are dietary additives.
In the current talk we will review the effects of dietary additives such as:
maltodextrins
carrageenans
 gums
emulsifiers
and the effects upon the microbiome and goblet cells.

Elucidate factors that help to make the successful transition from the bench to research group leader.