In these challenging times for all healthcare professionals, IBD Nurses continue to be an important part of the multidisciplinary team in managing patients with IBD. Many nurses have multiple roles and responsibilities and provide a variety of services. The exact extent and depth of care and services provided vary from country to country, depending on the education levels, the local requirements of the patients and the gastroenterology team, and the professional regulations in the individual county.

Antonino Spinelli © ECCO

This year, the European Crohn’s and Colitis Organisation (ECCO) and the European Society of Gastrointestinal and Abdominal Radiology (ESGAR) combined their expertise and resources to generate a Topical Review with a set of current practice positions to facilitate the correct and comprehensive reporting of imaging exams for Inflammatory Bowel Disease (IBD) patients.   

Imaging reports are one of the most important tools for clinicians, surgeons and technical staff, and this is particularly true for those caring for IBD patients, who often present with a variety of complicated clinical features. 

Our journey over the past year has been a remarkable one, and all of us have faced challenging times. As a result of the COVID-19 pandemic, this year’s ECCO Imaging Courses, including the Basic Imaging and Advanced Ultrasound Workshops, have had to move online as fully virtual meetings.

Konstantinos Karmiris  © ECCO

Owing to the COVID-19 pandemic, the 19^th ECCO IBD Intensive Course for Trainees will exceptionally take place in a virtual format on Friday, July 2, 2021 (one-day duration), one week prior to the start of the main ECCO Congress. The ECCO IBD Intensive Course for Trainees has become a tradition. It is the oldest educational initiative of ECCO, dating back to 2003, before the launch of the ECCO Congress, and is the cornerstone of the Education Committee’s activities.

Behrooz Alizadeh  © ECCO

Inflammatory Bowel Disease (IBD) is a chronic relapsing and remitting disease of the gut. IBD has a lifelong adverse impact on quality of life and imposes a significant burden on health care [1, 2]. The pathogenesis and course of IBD involve pathogenomic crosstalk among several complex internal components [3, 4], namely the genome [5], epigenome [3, 4], metabolome [3, 4, 6], immunome and microbiome [6–9]; this crosstalk is generally triggered through a set of external complex interactions among the exposome [10–13], dietome [14, 15], lifestyle, social and behavioural factors [16]. While some of these multi-level interactions trigger the disease, others drive the disease course. Therefore, in each IBD patient the disease arises through a (unique) combination of pathogenenomic (risk) factors or pathway that yield a specific set of disease manifestations and a specific disease course. In this context, an “individualized” therapy is required [17–19].

A NEUROEPITHELIAL APPROACH TO INFLAMMATORY BOWEL DISEASE

Roksana Maria Pirzgalska © Roksana Maria Pirzgalska

Aim of research

Deregulation of the gut mucosa is an under-appreciated aspect of Inflammatory Bowel Disease (IBD) and metabolic syndrome. We hypothesise that brain-derived signals modulate mucosal physiology by regulating both immune responses in the gut and the absorptive capacity of intestinal cells. We aim to understand the function of this proposed brain–gut circuit and to what extent this information can be harnessed from a clinical perspective.

A SYSTEMS BIOLOGY APPROACH FOR IDENTIFICATION OF HOST AND MICROBIAL MECHANISMS AND DRUGGABLE TARGETS FOR THE TREATMENT OF PSC-IBD

M. Nabil Quraishi © M. Nabil Quraishi

Aim of research

Primary sclerosing cholangitis (PSC) is a rare hepatobiliary manifestation of Inflammatory Bowel Disease (IBD) that is associated with significant and disproportionate unmet needs and a higher all-cause mortality compared with IBD alone. Unfortunately, no medical therapy has been proven to slow disease progression in PSC-IBD, and liver transplantation is the only life-saving intervention for patients.

We recently identified distinct mucosal transcriptomic profiles in PSC-IBD with regard to bile acid metabolism, bile acid signalling and a central role of enteric dysbiosis. Data from other groups have shown that oral vancomycin attenuates colonic inflammation and improves biochemical markers of cholestasis in PSC. In our study, we hypothesise that oral vancomycin attenuates colonic mucosal inflammation in PSC-IBD by restoring gut microbiota-mediated bile acid homeostatic pathways. We aim to identify druggable gut microbial and host molecular pathways associated with bile acid-mediated colonic mucosal inflammation in PSC-IBD.

DEFINING AND SUPPORTING MUCOSAL HEALING IN INFLAMMATORY BOWEL DISEASE

Charlotte Hedin © Charlotte Hedin

Aim of research

One goal of Ulcerative Colitis (UC) treatment is complete endoscopic/histological mucosal healing (MH). The treatments currently used to achieve MH almost universally act through immunosuppression, with side-effects of infection and cancer. Therapeutic strategies that directly promote MH are lacking, partly due to poor understanding of the dynamics and different phases of MH. Better knowledge of the stages of MH may also inform optimal timing of therapeutic interventions.

The aims of this project are to generate an in-depth dynamic molecular characterisation of patients with acute, active UC and to follow the development of this profile into either MH or eventual non-response with consequent surgery. The molecular data will be linked to detailed registration of diet during inflammation and healing and to durability of remission.

THE ROLE OF AUTOPHAGY IN LIMITING IBD-ASSOCIATED AIEC-INDUCED INTESTINAL INFLAMMATION

Shai Bel © Shai Bel

Aim of research

While the aetiology underlying the development of Inflammatory Bowel Diseases (IBD) is unclear, evidence points to an interaction between host genetics, such as mutations in autophagy genes, and environmental factors, such as bacterial infections. Multiple studies have identified an adherent-invasive Escherichia coli pathotype (AIEC) that attaches to intestinal epithelial cells (IECs) in patients with IBD but not in healthy subjects. It is thought that AIEC exploits the intestinal inflammation in patients with IBD to attach to the IECs, intensifying the pre-existing inflammation. Studies in vitro have shown that functional autophagy is crucial to eliminate AIEC infection. Here, we aim to identify how, and in which compartment of the intestine, autophagy protects the host from AIEC-associated pathologies in vivo and to determine whether artificially enhancing the autophagy process is a viable therapeutic avenue for patients with IBD and intestinal AIEC colonisation.

TISSUE-ASSOCIATED MICROBIAL AND CELLULAR DRIVERS OF RESOLUTION OF INFLAMMATION AND DISEASE EXACERBATION IN A LONG-TERM COHORT OF PAEDIATRIC CD PATIENTS

Tobias Schwerd ©  Tobias Schwerd

Aim of research

Inflammatory Bowel Diseases (IBD) are characterised by episodes of disease quiescence and disease exacerbation. The microbial and molecular events that result in long-lasting resolution of inflammation or the transition from IBD quiescence (mucosal healing) to active intestinal inflammation are unknown. Intestinal inflammation arises from a dysregulated response of tissue-resident immune cells, such as T cells, towards the intestinal microbiota. We aim to study longitudinal host–microbe interactions at the mucosal level as a strategy to identify microbial and molecular events associated with the resolution or re-activation of intestinal inflammation in individual paediatric patients with IBD.