Login to your account
Don’t have an account?
Create a Free Account
2017: Highlights
State of the Journal: CMGH’s Progress, Prospects, and Impact Factor
Cellular and Molecular Gastroenterology and Hepatology (CMGH) was established to create a forum for high-quality, mechanistic studies of the gastrointestinal tract, liver, and pancreas. CMGH has now completed its third full year of publication and has developed a reputation as a rigorous and highly regarded platform for basic and translational research. CMGH has also become known for a prompt, fair, and transparent review process in which authors are treated with respect and have access to editors.All Hands on Deck: Commensals, Th17 Cells, and Neutrophils Provide Short-term Compensation of Constitutive Permeability Defects Against Acute Infection
Although ample evidence has been generated that increased intestinal permeability contributes to many inflammatory and disease phenotypes, both in the intestines and in extra-intestinal sites such as the liver, it also has been shown in several model systems that a barrier defect alone generally is insufficient to induce chronic inflammatory conditions such as ulcerative colitis and Crohn’s disease. This is reflected in clinical data showing that a subset of healthy first-degree relatives of Crohn’s disease patients show increased intestinal permeability but do not go on to develop full-blown disease, even though increased permeability can serve as a predictor of disease relapse.Bacterial Autophagy: Offense and Defense at the Host–Pathogen Interface
Autophagy is a fundamental cellular process used for the turnover and recycling of cytosolic components and damaged organelles. Originally characterized as a response to cellular stress, it now is well established that autophagy also is used as a defensive mechanism to combat the infection of host cells by intracellular pathogens. However, although this defensive strategy does limit the proliferation of most pathogens within their host cells, successful pathogens have evolved countermeasures that subvert or circumvent the autophagic response.Colonic Microbiota Encroachment Correlates With Dysglycemia in Humans
Mucoid structures that coat the epithelium play an essential role in keeping the intestinal microbiota at a safe distance from host cells. Encroachment of bacteria into the normally almost-sterile inner mucus layer has been observed in inflammatory bowel disease and in mouse models of colitis. Moreover, such microbiota encroachment has also been observed in mouse models of metabolic syndrome, which are associated low-grade intestinal inflammation. Hence, we investigated if microbiota encroachment might correlate with indices of metabolic syndrome in humans.Insights From the Crypt: Regionalization, Adaptation, and Renewal of the Intestinal Epithelium
The current issue of Cellular and Molecular Gastroenterology and Hepatology presents 3 important studies that further our understanding of intestinal epithelial regionalization, adaptation, and maintenance by using both rare human pediatric ileal samples and advanced mouse genetic models.Uncovering Pathogenic Mechanisms of Inflammatory Bowel Disease Using Mouse Models of Crohn’s Disease–Like Ileitis: What is the Right Model?
Crohn’s disease and ulcerative colitis, together known as inflammatory bowel disease, are debilitating chronic disorders of unknown cause and cure. Our evolving understanding of these pathologies is enhanced greatly by the use of animal models of intestinal inflammation that allow in vivo mechanistic studies, preclinical evaluation of new therapies, and investigation into the causative factors that underlie disease pathogenesis. Several animal models, most commonly generated in mice, exist for the study of colitis.Notch as a Driver of Gastric Epithelial Cell Proliferation
The gastric epithelium is sustained by a population of stem cells that replenish the various mature epithelial lineages throughout adulthood. Regulation of stem and progenitor cell proliferation occurs via basic developmental signaling pathways, including the Notch pathway, which recently was described to promote gastric stem cell proliferation in both mice and human beings. Current cancer theory proposes that adult stem cells that maintain gastrointestinal tissues accumulate mutations that promote cancerous growth, and that basic signaling pathways, such as Notch, which stimulate stem cell proliferation, can promote tumorigenesis.Tightening the Case for Gut Microbiota in Autism-Spectrum Disorder
Autism-spectrum disorder (ASD) is a developmental behavioral disorder often accompanied and aggravated by a range of gastrointestinal and cognitive dysfunction. The concern for ASD reflects its increasing incidence and the disproportionate burden of this and other cognitive disorders on those affected and the family and community around them. Is there a role for us to help from the distant fields of gastroenterology and hepatology?Thymic Stromal Lymphopoietin: To Cut a Long Story Short
Thymic stromal lymphopoietin (TSLP) was identified more than 20 years ago as a secreted factor of a mouse thymic stromal cell line; later, a human orthologue was also identified. The signaling pathway triggered by TSLP has been extensively studied, and upregulation of the cytokine itself is linked to the pathogenesis of numerous Th2-related diseases, including atopic dermatitis, asthma, allergic responses, as well as certain types of cancers. On the other hand, TSLP mediates several immune homeostatic functions in both the gut and the thymus.Mitogen-activated Protein Kinase Kinase Activity Maintains Acinar-to-Ductal Metaplasia and Is Required for Organ Regeneration in Pancreatitis
Mitogen-activated protein kinase (MAPK) signaling in the exocrine pancreas has been extensively studied in the context of pancreatic cancer, where its potential as a therapeutic target is limited by acquired drug resistance. However, its role in pancreatitis is less understood. We investigated the role of mitogen-activated protein kinase kinase (MEK)-initiated MAPK signaling in pancreatitis to determine the potential for MEK inhibition in treating pancreatitis patients.Interferon-Alpha Promotes Th1 Response and Epithelial Apoptosis via Inflammasome Activation in Human Intestinal Mucosa
Several lines of investigation suggest that interferon (IFN) alpha can alter human intestinal mucosa homeostasis. These include the endogenous production of IFN alpha in celiac disease or inflammatory bowel diseases, as well as the occurrence of intestinal side effects of exogenous IFN alpha used as a therapeutic tool. Here, we present an ex vivo translational approach to investigate the effects of IFN alpha on the human normal intestinal mucosa, as well as its underlying mechanisms.
Copyright © 2023 Elsevier Inc. except certain content provided by third parties. The content on this site is intended for healthcare professionals.
