81. Purified oat protein can trigger acute symptoms linked to immune activation in coeliac disease patients but not histological deterioration.
作者: Melinda Y Hardy.;Amy K Russell.;Lee M Henneken.;Greg Tanner.;Ferenc Bekes.;Ian Brown.;Allan Motyer.;Sam W Z Olechnowicz.;Hugh H Reid.;Jamie Rossjohn.;Jason A Tye-Din.
来源: Gut. 2025年
Oat ingestion in coeliac disease (CD) is generally regarded as safe but can trigger enteropathy and T cells specific for oat avenin in the gut and blood of some individuals.
82. Gut microbiota-related neuroinflammation at the crossroad of food reward alterations: implications for eating disorders.
The link between gut microbiome and eating behaviours, especially palatable food intake, is a growing focus of scientific investigation. The complex ecosystem of microorganisms in the gut influences host metabolism, immune function and neurobehavioural signalling. This review explores the role of neuroinflammation in dysregulations of food-induced reward signalling and the potential causal role of the gut microbiota on these proinflammatory processes. Particular attention is given to eating disorders (ED, specifically anorexia nervosa, binge eating disorder and bulimia nervosa) and potential links with the gut microbiota, food reward alterations and neuroinflammation. Finally, we propose gut microbiota modulation as a promising therapeutic strategy in food reward alterations and ED.
87. Histology of subepithelial lesions (SELs) in the gastrointestinal tract-resected endoscopic: a database study of 4901 patients.
作者: Zhipeng Qi.;Enpan Xu.;Shuchang Xu.;Leiming Xu.;XiaoBo Li.;Liang Zhong.;Dongli He.;Pinghong Zhou.;Zhendong Jin.;Yunshi Zhong.; .
来源: Gut. 2025年 88. Carbon footprinting and environmental impact of gastrointestinal endoscopy procedures at a tertiary care institution: a prospective multi-dimensional assessment.
作者: Hardik Rughwani.;Rakesh Kalapala.;Anudeep Katrevula.;Nitin Jagtap.;Madhav Desai.;Sara Teles de Campos.;Mohan Ramchandani.;Sundeep Lakhtakia.;Rupjyoti Talukdar.;Santosh Darisetty.;Sana Fatima Memon.;Guduru Venkat Rao.;Marco Bruno.;Prateek Sharma.;D Nageshwar Reddy.
来源: Gut. 2025年
Given the imperative to combat climate change, reducing the healthcare sector's implications on the environment is crucial.
89. Single-cell omics in inflammatory bowel disease: recent insights and future clinical applications.
Inflammatory bowel diseases (IBDs), which include ulcerative colitis (UC) and Crohn's disease (CD), are chronic conditions characterised by inflammation of the intestinal tract. Alterations in virtually all intestinal cell types, including immune, epithelial and stromal cells, have been described in these diseases. The study of IBD has historically relied on bulk transcriptomics, but this method averages signals across diverse cell types, limiting insights. Single-cell omic technologies overcome the intrinsic limitations of bulk analysis and reveal the complexity of multicellular tissues at a cell-by-cell resolution. Within healthy and inflamed intestinal tissues, single-cell omics, particularly single-cell RNA sequencing, have contributed to uncovering novel cell types and cell functions linked to disease activity or the development of complications. Collectively, these results help identify therapeutic targets in difficult-to-treat complications such as fibrostenosis, creeping fat accumulation, perianal fistulae or inflammation of the pouch. More recently, single-cell omics have gradually been adopted in studies to understand therapeutic responses, identify mechanisms of drug failure and potentially develop predictors with clinical utility. Although these are early days, such studies lay the groundwork for the implementation in clinical practice of new technologies in diagnostics, monitoring and prediction of disease prognosis. With this review, we aim to provide a comprehensive survey of the studies that have applied single-cell omics to the study of UC or CD, and offer our perspective on the main findings these studies contribute. Finally, we discuss the limitations and potential benefits that the integration of single-cell omics into clinical practice and drug development could offer.
90. Dysbiotic oral microbiota-derived kynurenine, induced by chronic restraint stress, promotes head and neck squamous cell carcinoma by enhancing CD8+ T cell exhaustion.
作者: Fangzhi Lou.;Li Yan.;Shihong Luo.;Yunmei Dong.;Jingyi Xu.;Ning Kang.;Haiyang Wang.;Yiyun Liu.;Juncai Pu.;Bing Yang.;Richard D Cannon.;Peng Xie.;Ping Ji.;Xin Jin.
来源: Gut. 2025年
Chronic restraint stress (CRS) is a tumour-promoting factor. However, the underlying mechanism is unknown.
91. Glucocorticoid receptor suppresses GATA6-mediated RNA polymerase II pause release to modulate classical subtype identity in pancreatic cancer.
作者: Thomas L Ekstrom.;Raya M Rosok.;Amro M Abdelrahman.;Christina Parassiadis.;Meghana Manjunath.;Marianna Y Dittrich.;Xin Wang.;Ana P Kutschat.;Akshay Kanakan.;Ashish Rajput.;Nadine Schacherer.;Teodora Lukic.;Danielle M Carlson.;Julia Thiel.;Waltraut Kopp.;Philipp Stroebel.;Volker Ellenrieder.;Jochen Gaedcke.;Meng Dong.;Zeynab Najafova.;Mark J Truty.;Elisabeth Hessmann.;Steven A Johnsen.
来源: Gut. 2025年
Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal cancer with a 5-year survival rate of 12%. It has two major molecular subtypes: classical and basal, regulated by the master transcription factors (MTFs) GATA6 and ΔNp63, respectively.
93. Low-coverage whole genome sequencing of low-grade dysplasia strongly predicts advanced neoplasia risk in ulcerative colitis.
作者: Ibrahim Al Bakir.;Kit Curtius.;George D Cresswell.;Heather E Grant.;Nadia Nasreddin.;Kane Smith.;Salpie Nowinski.;Qingli Guo.;Hayley L Belnoue-Davis.;Jennifer Fisher.;Theo Clarke.;Christopher Kimberley.;Maximilian Mossner.;Philip D Dunne.;Maurice B Loughrey.;Ally Speight.;James E East.;Nicholas A Wright.;Manuel Rodriguez-Justo.;Marnix Jansen.;Morgan Moorghen.;Ann-Marie Baker.;Simon J Leedham.;Ailsa L Hart.;Trevor A Graham.
来源: Gut. 2025年74卷5期740-751页
The risk of developing advanced neoplasia (AN; colorectal cancer and/or high-grade dysplasia) in ulcerative colitis (UC) patients with a low-grade dysplasia (LGD) lesion is variable and difficult to predict. This is a major challenge for effective clinical management.
95. In vitro microbiota model recapitulates and predicts individualised sensitivity to dietary emulsifier.
作者: Héloïse Rytter.;Sabrine Naimi.;Gary Wu.;Jim Lewis.;Maeva Duquesnoy.;Lucile Vigué.;Olivier Tenaillon.;Eugeni Belda.;Marta Vazquez-Gomez.;Nina Touly.;Djésia Arnone.;Fuhua Hao.;Ruth E Ley.;Karine Clément.;Laurent Peyrin-Biroulet.;Andrew D Patterson.;Andrew T Gewirtz.;Benoit Chassaing.
来源: Gut. 2025年74卷5期761-774页
Non-absorbed dietary emulsifiers, including carboxymethylcellulose (CMC), directly disturb intestinal microbiota, thereby promoting chronic intestinal inflammation in mice. A randomised controlled-feeding study (Functional Research on Emulsifiers in Humans, FRESH) found that CMC also detrimentally impacts intestinal microbiota in some, but not all, healthy individuals.
96. Fasting-mimicking diet-enriched Bifidobacterium pseudolongum suppresses colorectal cancer by inducing memory CD8+ T cells.
作者: Ke Nan.;Ziwen Zhong.;Ying Yue.;Yang Shen.;Hao Zhang.;Zhiqiang Wang.;Kameina Zhuma.;Baichao Yu.;Ying Fu.;Luman Wang.;Xingfeng Sun.;Mengdi Qu.;Zhaoyuan Chen.;Miaomiao Guo.;Jie Zhang.;Yiwei Chu.;Ronghua Liu.;Changhong Miao.
来源: Gut. 2025年74卷5期775-786页
Fasting-mimicking diet (FMD) boosts the antitumour immune response in patients with colorectal cancer (CRC). The gut microbiota is a key host immunity regulator, affecting physiological homeostasis and disease pathogenesis.
97. Risk factors for pancreatic cancer in individuals with intraductal papillary mucinous neoplasms and no high-risk stigmata during up to 5 years of surveillance: a prospective longitudinal cohort study.
作者: Tsuyoshi Hamada.;Hiroki Oyama.;Daniel Nevo.;Shuichi Tange.;Shinya Takaoka.;Yoshikuni Kawaguchi.;Kazunaga Ishigaki.;Kensaku Noguchi.;Tomotaka Saito.;Tatsuya Sato.;Tatsunori Suzuki.;Naminatsu Takahara.;Mariko Tanaka.;Kiyoshi Hasegawa.;Tetsuo Ushiku.;Yousuke Nakai.;Maxim S Petrov.;Mitsuhiro Fujishiro.; .
来源: Gut. 2025年
Cyst size, its growth rate, and diameter of the main pancreatic duct (MPD) are all associated with pancreatic carcinoma prevalence in intraductal papillary mucinous neoplasms (IPMNs).
98. Predictors of response to low-dose amitriptyline for irritable bowel syndrome and efficacy and tolerability according to subtype: post hoc analyses from the ATLANTIS trial.
作者: Alexandra Wright-Hughes.;Pei-Loo Ow.;Sarah L Alderson.;Matthew J Ridd.;Robbie Foy.;Felicity L Bishop.;Matthew Chaddock.;Catherine Fernandez.;Elspeth A Guthrie.;Delia P Muir.;Christopher A Taylor.;Amanda J Farrin.;Hazel A Everitt.;Alexander C Ford.
来源: Gut. 2025年74卷5期728-739页
Low-dose amitriptyline, a tricyclic antidepressant (TCA), was superior to placebo for irritable bowel syndrome (IBS) in the AmitripTyline at Low-dose ANd Titrated for Irritable bowel syndrome as Second-line treatment (ATLANTIS) trial.
100. Metabolic dysfunction-associated steatotic liver disease in children.
Metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as non-alcoholic fatty liver disease, is the most common cause of chronic liver disease in children. MASLD encompasses a spectrum of liver disease and can be severe, with 10% of affected children presenting with advanced fibrosis. While biopsy remains the most accurate method for diagnosing and staging the disease, MRI proton density fat fraction and magnetic resonance elastography are the most reliable non-invasive measures for assessing steatosis and fibrosis, respectively. MASLD is associated with multiple comorbidities including type 2 diabetes, hypertension, dyslipidaemia, decreased bone mineral density, obstructive sleep apnoea, anxiety and depression. Currently, there are no pharmacological treatments available for children, highlighting the urgent need for paediatric clinical trials. A diet low in free sugars is promising for reducing steatosis and decreasing alanine aminotransferase, a surrogate marker for hepatic inflammation. Emerging data indicate that steatosis can be present in children under 6 years of age, which was previously considered rare. The intricate interplay of genetics may inform future therapeutics and prognostication, with the PNPLA3 gene showing the most evidence for association with the risk and severity of steatotic liver disease and steatohepatitis. MASLD is a complex disease affecting one in ten children and is associated with increased early mortality risk. More dedicated studies are needed in children to advance our understanding of this disease and find effective treatments.
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