Monocyte-derived macrophages as crucial players in the resolution of inflammation and tissue repair in Inflammatory Bowel Disease  

Sales Ibiza © Sales Ibiza

Background

Inflammatory Bowel Disease (IBD) is characterised by chronic inflammation of the gastrointestinal tract leading to debilitating symptoms. No curative therapies are currently available for IBD, with the consequence that the disease has a significant impact on the emotional, financial and social status of patients and their families. Although most studies conducted on IBD over the past few decades have investigated abnormal adaptive immunity, the focus has recently shifted towards alterations in innate immune response. Recent data suggest a causal link between defects in the resolution of inflammation associated with impaired bacterial clearance, excessive cytokine secretion and altered monocyte-macrophage (Mφ) transition in patients with IBD.

Deciphering the gut-specific B cell response in Inflammatory Bowel Disease (IBD)  

Mathieu Uzzan © Mathieu Uzzan

Aim of the research

Given that there is a large complement of mucosal B cells that plays a pivotal role in the regulation of the microbiome and in mucosal homeostasis, it is likely that they play an important but yet understudied role in the pathogenesis of IBD. Therefore, we hypothesize that mucosal inflammation as seen in IBD will induce a B cell response with homeostatic and perhaps pathogenic properties.

Investigation of the role of Par4-associated cell polarity and associated barrier defects in Inflammatory Bowel Diseases  

Federica Branchi © Federica Branchi

Aim of the research

In Inflammatory Bowel Diseases (IBD), epithelial barrier defects occur as a consequence of chronic inflammation. Recent research has suggested that cell polarity alterations may be upstream of barrier defects and additionally play a role in IBD-associated carcinogenesis (colitis-associated and small intestinal carcinoma). Par4 is a gene encoding a protein crucial in the development of cell polarity. LKB1, its human homologue, is mutated in Peutz-Jeghers syndrome (PJS), a genetic condition characterised by a higher risk of epithelial cancers. Considering the pivotal role of Par4/LKB1 in the development of epithelial cell polarity, this project aims to assess its involvement in IBD-associated barrier defects and carcinogenesis.

Viktor Domislović  © Viktor Domislović

Cumulative burden of inflammation predicts colorectal neoplasia risk in Ulcerative Colitis: A large single-centre study

Choi CR, Al Bakir I, Ding NJ, Lee GH, Askari A, Warusavitarne J, Moorghen M, Humphries A, Ignjatovic-Wilson A, Thomas-Gibson S, Saunders BP, Rutter MD, Graham TA, Hart AL
Gut. 2017 Nov 17. pii: gutjnl-2017-314190. doi: 10.1136/gutjnl-2017-314190.

Valentina Petito © Valentina Petito

Uncoupling of mucosal gene regulation, mRNA splicing and adherent microbiota signatures in Inflammatory Bowel Disease

Häsler R, Sheibani-Tezerji R, Sinha A, Barann M, Rehman A, Esser D, Aden K, Knecht C, Brandt B, Nikolaus S, Schäuble S, Kaleta C, Franke A, Fretter C, Müller W, Hütt MT, Krawczak M, Schreiber S, Rosenstiel P
Gut. 2017;66:2087–2097. doi:10.1136/gutjnl-2016-311651

Nuha Yassin © ECCO

With the Y-ECCO Interview corner, we travel the world and share the thoughts of some of the most inspirational IBD leaders. Today we travel to Australia in order to share the IBD journey of a very successful and inspirational IBD leader, Professor Jane Andrews, who is head of the IBD service and Education in the Department of Gastroenterology and Hepatology at The Royal Adelaide Hospital in Australia and a clinical professor at the School of Medicine, University of Adelaide.

Nuha Yassin © ECCO

Dear Y-ECCO Friends,

Greetings fellow Y-ECCOs. I hope you are all enjoying some warmth after the prolonged winter. The Young ECCO Committee (Y-ECCO) has been using the cold winter time well, wrapped up indoors and brewing up a couple of brand new hot beverages for you as we continue to strive to provide Y-ECCO Members with the best possible offers.

Magali Svrcek © ECCO

In addition to the “classical” pathway of colorectal carcinogenesis, involving development of cancer from an adenomatous precursor lesion, an alternative pathway, the serrated pathway, is now recognised to exist, and it is estimated that approximately 30% of colorectal cancers (CRC) arise via this alternative pathway [1]. In the last WHO classification, serrated polyps were classified as (i) hyperplastic polyps (HP), (ii) sessile serrated adenoma/polyps (SSA/P), with or without dysplasia, and (iii) traditional serrated adenomas (TSA). The possibility of a serrated pathway has also been suggested in colorectal carcinoma complicating Inflammatory Bowel Disease (IBD) [2–4]. Little is known concerning immunohistochemical and molecular features of serrated lesions in IBD: Data are limited to small series of patients or case reports and findings are controversial due to the rarity of the cases. However, the clinical, pathological and biological characteristics of serrated polyps in patients with IBD do seem to resemble those of their sporadic counterparts.

Lissy de Ridder © ECCO

Paediatric Inflammatory Bowel Disease (IBD) accounts for 10%–15% of all incident cases of IBD, while the incidence in children under 10 years old is rising most rapidly [1, 2]. Children and adolescents present with a more severe phenotype of disease and have both higher and unique risks (e.g. fistulising disease, growth failure, pubertal delay) and a longer disease duration, given that IBD is a lifelong disease. 

Yves Panis © ECCO

As Chair of the S-ECCO Committee, it is my pleasure to introduce two newly elected members for 2018: Christianne Buskens and Hagit Tulchinsky. Thus, as of today, the members of the S-ECCO Committee are: Antonino Spinelli (Milan, Italy; member until March 2019), Yves Panis (Clichy, France; Chair until February 2020), Michel Adamina (Winterthur, Switzerland; member until February 2020) and Christianne Buskens and Hagit Tulchinsky. Both Christianne and Hagit will stay for 3 years, until February 2021.