Duodenal adenomas have malignant potential, yet the drivers of duodenal tumorigenesis remain unclear. Duodenal adenomas robustly develop in villin-TLR4 mice, a transgenic mouse model of increased innate immune signaling in the intestinal epithelium. Here, we sought to test the contributions of the microbiota and bile acids to duodenal adenoma development.

IL-1β is a key cytokine in hepatitis-related inflammation, but its role in metabolic dysfunction-associated steatotic liver disease (MASLD) or steatohepatitis (MASH) remains unclear. This study investigated IL-1β-mediated interactions in non-parenchymal liver cells to elucidate their contributions to pathological MASH progression.

Fibrostenosis is a major complication of Crohn's disease (CD) characterized by intestinal remodeling and excessive extracellular matrix (ECM) deposition. A prominent feature is bowel wall muscularization, involving expansion of submucosal myoid cells and muscularis propria (MP) smooth muscle cell (SMC) hyperplasia. However, the cellular identity and molecular mechanisms underlying submucosal myoid cell hyperplasia remain poorly characterized.

The gut-liver axis plays a critical role in metabolic dysfunction-associated steatohepatitis (MASH). Osteopontin (OPN, encoded by SPP1) is implicated in chronic liver disease; however, its expression in intestinal epithelial cells (IECs) and role in MASH remain unclear.

Mechanisms of hepatitis C virus (HCV) adaptation and escape from broadly neutralizing antibodies (bNAbs) have been primarily studied in vitro. Here, we used a previously developed in vivo adapted J6/JFH1 virus and the highly bNAb sensitive hypervariable region 1 (HVR1) deleted variant, J6/JFH1, to study adaptation and bNAb AR5A escape in the HCV-permissive human-liver chimeric mouse model.

SNX27, member of the sorting nexin (SNX) family, carries a unique PDZ domain and mediates recycling of endocytosed transmembrane proteins. SNX27 is critical for neurodevelopmental processes, however its role in intestine remains unexplored. We aim to determine the previously unknown roles of SNX27 in regulating intestinal homeostasis, epithelial barrier integrity, and inflammatory responses.

Potassium and chloride efflux have been reported to regulate NLRP3 inflammasome activation. Aberrant activation of NLRP3 inflammasome causes autoimmune and chronic inflammatory diseases. The Na-K-2Cl cotransporter (NKCC1) maintains the intracellular concentrations of sodium, potassium, and chloride. Here we ask whether NKCC1 modulates NLRP3 inflammasome activation.

Breast milk contains abundant glutamine and glutamate, yet their roles in neonatal gut health remain controversial. We aimed to investigate how these amino acids influence neonatal enteritis and the underlying mechanisms.

Abstinence is beneficial for patients with alcohol-associated liver disease (ALD), but disease resolution after alcohol cessation occurs slowly and only in a subset of patients. We aimed to study the mechanisms of ALD resolution using spatial transcriptomics.

Gastric cancer is the fifth most common cancer worldwide. Men are disproportionately affected by gastric cancer, which ranks as the fourth most common cancer in men compared to eighth in women. Chronic inflammation driven by Helicobacter pylori infection remains the leading gastric cancer risk factor. Evidence suggests that sex hormones shape sex differences in infection outcomes and cancer susceptibility. This study investigates how androgens influence the gastric inflammatory response to Helicobacter infection and contribute to sex disparities in pre-dysplastic disease progression.

Acute drug-induced liver injury (DILI) is a major cause of acute liver dysfunction and even liver failure. Peritoneal macrophages have been reported to invade into the injured liver for tissue repair. Herein, we aimed to investigate the role of autophagy-related 16 like 1 gene (ATG16L1) in regulating the reparative function of peritoneal macrophages during DILI caused by acetaminophen (APAP).

Hepatic ischemia reperfusion injury (IRI) is unavoidable in most liver operations and is associated with poor patient and graft outcomes in the setting of liver transplantation. However, there are no pharmacological interventions available for treatment of IRI. Prior work has demonstrated that liver IRI leads to hepatic lipid accumulation, suggesting that increased adipocyte lipolytic rates may contribute to hepatic steatosis. Inhibition of adipose triglyceride lipase (ATGL), the rate limiting enzyme involved in triglyceride hydrolysis, may be beneficial in cardiac injury and alcoholic liver disease, but its role in liver IRI has not been investigated. Our objective was to assess the effects of inhibition of adipose tissue lipolysis in the setting of liver IRI.

Localised acidification from immune cell infiltration and heightened glycolysis contributes to colitis pathology by activating acid-sensing receptors such as GPR68, a proton-sensing GPCR expressed on immune and stromal cells. Single-cell RNAseq analysis revealed GPR68 is also expressed in colonic sensory neurons, prompting us to investigate its role in acid-induced colonic nociception.