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Cellular and Molecular Gastroenterology and Hepatology

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https://www.readbyqxmd.com/read/28795125/the-microbiome-activates-cd4-t-cell-mediated-immunity-to%C3%A2-compensate-for-increased-intestinal-permeability
#1
Karen L Edelblum, Gil Sharon, Gurminder Singh, Matthew A Odenwald, Anne Sailer, Severine Cao, Sarina Ravens, Irene Thomsen, Kamal El Bissati, Rima McLeod, Chen Dong, Sandeep Gurbuxani, Immo Prinz, Sarkis K Mazmanian, Jerrold R Turner
BACKGROUND & AIMS: Despite a prominent association, chronic intestinal barrier loss is insufficient to induce disease in human subjects or experimental animals. We hypothesized that compensatory mucosal immune activation might protect individuals with increased intestinal permeability from disease. We used a model in which intestinal barrier loss is triggered by intestinal epithelial-specific expression of constitutively active myosin light chain kinase (CA-MLCK). Here we asked whether constitutive tight junction barrier loss impacts susceptibility to enteric pathogens...
September 2017: Cellular and Molecular Gastroenterology and Hepatology
https://www.readbyqxmd.com/read/28795124/the-quest-for-relevant-hepatocellular-carcinoma-biomarkers
#2
EDITORIAL
Jin U Kim, I Jane Cox, Simon D Taylor-Robinson
No abstract text is available yet for this article.
September 2017: Cellular and Molecular Gastroenterology and Hepatology
https://www.readbyqxmd.com/read/28752115/acinar-to-ductal-metaplasia-induced-by-transforming-growth-factor-beta-facilitates-kras-g12d-driven-pancreatic-tumorigenesis
#3
Nicolas Chuvin, David F Vincent, Roxane M Pommier, Lindsay B Alcaraz, Johann Gout, Cassandre Caligaris, Karam Yacoub, Victoire Cardot, Elodie Roger, Bastien Kaniewski, Sylvie Martel, Celia Cintas, Sophie Goddard-Léon, Amélie Colombe, Julie Valantin, Nicolas Gadot, Emilie Servoz, Jennifer Morton, Isabelle Goddard, Anne Couvelard, Vinciane Rebours, Julie Guillermet, Owen J Sansom, Isabelle Treilleux, Ulrich Valcourt, Stéphanie Sentis, Pierre Dubus, Laurent Bartholin
BACKGROUND & AIMS: Transforming growth factor beta (TGFβ) acts either as a tumor suppressor or as an oncogene, depending on the cellular context and time of activation. TGFβ activates the canonical SMAD pathway through its interaction with the serine/threonine kinase type I and II heterotetrameric receptors. Previous studies investigating TGFβ-mediated signaling in the pancreas relied either on loss-of-function approaches or on ligand overexpression, and its effects on acinar cells have so far remained elusive...
September 2017: Cellular and Molecular Gastroenterology and Hepatology
https://www.readbyqxmd.com/read/28752114/do-animal-models-of-acute-pancreatitis-reproduce-human%C3%A2-disease
#4
REVIEW
Fred S Gorelick, Markus M Lerch
Acute pancreatitis is currently the most common cause of hospital admission among all nonmalignant gastrointestinal diseases. To understand the pathophysiology of the disease and as a potential step toward developing targeted therapies, attempts to induce the disease experimentally began more than 100 years ago. Recent decades have seen progress in developing new experimental pancreatitis models as well as elucidating many underlying cell biological and pathophysiological disease mechanisms. Some models have been developed to reflect specific causes of acute pancreatitis in human beings...
September 2017: Cellular and Molecular Gastroenterology and Hepatology
https://www.readbyqxmd.com/read/28752113/2017-aga-council-section-research-mentor-awardees
#5
EDITORIAL
(no author information available yet)
No abstract text is available yet for this article.
September 2017: Cellular and Molecular Gastroenterology and Hepatology
https://www.readbyqxmd.com/read/28660242/bacterial-autophagy-offense-and-defense-at-the-host-pathogen-interface
#6
REVIEW
James E Casanova
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...
September 2017: Cellular and Molecular Gastroenterology and Hepatology
https://www.readbyqxmd.com/read/28649594/specific-macronutrients-exert-unique-influences-on-the-adipose-liver-axis-to-promote-hepatic-steatosis-in-mice
#7
Caroline C Duwaerts, Amin M Amin, Kevin Siao, Chris Her, Mark Fitch, Carine Beysen, Scott M Turner, Amanda Goodsell, Jody L Baron, James P Grenert, Soo-Jin Cho, Jacquelyn J Maher
BACKGROUND & AIMS: The factors that distinguish metabolically healthy obesity from metabolically unhealthy obesity are not well understood. Diet has been implicated as a determinant of the unhealthy obesity phenotype, but which aspects of the diet induce dysmetabolism are unknown. The goal of this study was to investigate whether specific macronutrients or macronutrient combinations provoke dysmetabolism in the context of isocaloric, high-energy diets. METHODS: Mice were fed 4 high-energy diets identical in calorie and nutrient content but different in nutrient composition for 3 weeks to 6 months...
September 2017: Cellular and Molecular Gastroenterology and Hepatology
https://www.readbyqxmd.com/read/28649593/colonic-microbiota-encroachment-correlates-with-dysglycemia-in-humans
#8
Benoit Chassaing, Shreya M Raja, James D Lewis, Shanthi Srinivasan, Andrew T Gewirtz
BACKGROUND AND AIMS: 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...
September 2017: Cellular and Molecular Gastroenterology and Hepatology
https://www.readbyqxmd.com/read/28593188/barrett-s-stem-cells-as-a-unique-and-targetable%C3%A2-entity
#9
Wa Xian, Frank McKeon
Although metaplasias have always attracted because of their strangeness, it is now clear they represent precursors for some of the most intractable human cancers. Despite this notoriety, they remain curiously understudied, and even their origins have been the subject of acrimonious debate stretching back to Virchow in the 19th century. Barrett's esophagus, with its high incidence, easy endoscopic access, and strong link to esophageal adenocarcinoma, would seem an ideal opportunity to address the origin problem...
July 2017: Cellular and Molecular Gastroenterology and Hepatology
https://www.readbyqxmd.com/read/28593187/the-esophageal-squamous-epithelial-cell-still-a-reasonable-candidate-for-the%C3%A2-barrett-s-esophagus-cell-of%C3%A2-origin
#10
David H Wang
Barrett's esophagus is the metaplastic change of the squamous epithelium lining the distal esophagus into an intestinalized columnar epithelium that predisposes to esophageal adenocarcinoma development. The cell that gives rise to Barrett's esophagus has not been identified definitively, although several sources for the Barrett's esophagus cell of origin have been postulated. One possible source is a fully differentiated squamous epithelial cell or a squamous epithelial progenitor or stem cell native to the esophagus that, through molecular reprogramming, either transdifferentiation or transcommitment, could give rise to an intestinalized columnar cell...
July 2017: Cellular and Molecular Gastroenterology and Hepatology
https://www.readbyqxmd.com/read/28593186/origin-of-barrett-s-epithelium-esophageal-submucosal-glands
#11
Katherine S Garman
The origin of the progenitor cell for Barrett's esophagus remains a major unsolved mystery. Understanding the source of this progenitor may improve strategies to prevent the development of esophageal adenocarcinoma. Esophageal submucosal glands (ESMGs) and ducts may serve as a potential source of progenitor cells that respond to esophageal injury. Through the use of human histologic and molecular analysis, ESMGs and ducts have been described in physical continuity with areas of columnar esophagus, and shared mutations have been described between ESMG ducts and Barrett's esophagus...
July 2017: Cellular and Molecular Gastroenterology and Hepatology
https://www.readbyqxmd.com/read/28593185/induction-of-colonic-regulatory-t-cells-by-mesalamine-by-activating-the-aryl-hydrocarbon-receptor
#12
Kyoko Oh-Oka, Yuko Kojima, Koichiro Uchida, Kimiko Yoda, Kayoko Ishimaru, Shotaro Nakajima, Jun Hemmi, Hiroshi Kano, Yoshiaki Fujii-Kuriyama, Ryohei Katoh, Hiroyuki Ito, Atsuhito Nakao
BACKGROUND & AIMS: Mesalamine is a first-line drug for treatment of inflammatory bowel diseases (IBD). However, its mechanisms are not fully understood. CD4(+) Foxp3(+) regulatory T cells (Tregs) play a potential role in suppressing IBD. This study determined whether the anti-inflammatory activity of mesalamine is related to Treg induction in the colon. METHODS: We examined the frequencies of Tregs in the colons of wild-type mice, mice deficient for aryl hydrocarbon receptor (AhR(-/-) mice), and bone marrow-chimeric mice lacking AhR in hematopoietic cells (BM-AhR(-/-) mice), following oral treatment with mesalamine...
July 2017: Cellular and Molecular Gastroenterology and Hepatology
https://www.readbyqxmd.com/read/28593184/epigenetics-and-liver-fibrosis
#13
REVIEW
Eva Moran-Salvador, Jelena Mann
Liver fibrosis arises because prolonged injury combined with excessive scar deposition within hepatic parenchyma arising from overactive wound healing response mediated by activated myofibroblasts. Fibrosis is the common end point for any type of chronic liver injury including alcoholic liver disease, nonalcoholic fatty liver disease, viral hepatitis, and cholestatic liver diseases. Although genetic influences are important, it is epigenetic mechanisms that have been shown to orchestrate many aspects of fibrogenesis in the liver...
July 2017: Cellular and Molecular Gastroenterology and Hepatology
https://www.readbyqxmd.com/read/28593183/columnar-metaplasia-in-three-types-of-surgical-mouse-models-of-esophageal-reflux
#14
Fabio Terabe, Susumu Aikou, Junko Aida, Nobutake Yamamichi, Michio Kaminishi, Kaiyo Takubo, Yasuyuki Seto, Sachiyo Nomura
BACKGROUND AND AIMS: Esophageal adenocarcinoma develops in the setting of gastroesophageal reflux and columnar metaplasia in distal esophagus. Columnar metaplasia arising in gastroesophageal reflux models has developed in rat; however, gastroesophageal reflux models in mice have not been well-characterized. METHODS: One hundred thirty-five C57Bl/6J mice aged 8 weeks old were divided into the following operations: esophagogastrojejunostomy (side-to-side) (EGJ), esophageal separation and esophagojejunostomy (end-to-side) (EJ), and EJ and gastrectomy (end-to-side) (EJ/TG)...
July 2017: Cellular and Molecular Gastroenterology and Hepatology
https://www.readbyqxmd.com/read/28593182/the-circadian-clock-gene-bmal1-coordinates-intestinal%C3%A2-regeneration
#15
Kyle Stokes, Abrial Cooke, Hanna Chang, David R Weaver, David T Breault, Phillip Karpowicz
BACKGROUND & AIMS: The gastrointestinal syndrome is an illness of the intestine caused by high levels of radiation. It is characterized by extensive loss of epithelial tissue integrity, which initiates a regenerative response by intestinal stem and precursor cells. The intestine has 24-hour rhythms in many physiological functions that are believed to be outputs of the circadian clock: a molecular system that produces 24-hour rhythms in transcription/translation. Certain gastrointestinal illnesses are worsened when the circadian rhythms are disrupted, but the role of the circadian clock in gastrointestinal regeneration has not been studied...
July 2017: Cellular and Molecular Gastroenterology and Hepatology
https://www.readbyqxmd.com/read/28560293/isthmus-stem-cells-are-the-origins-of-metaplasia-in-the-gastric-corpus
#16
Yoku Hayakawa, James G Fox, Timothy C Wang
The acquisition of genetic/epigenetic mutations in long-lived gastrointestinal stem cells leads to the development of cancer, as well as precancerous lesions such as metaplasia and dysplasia. In the proximal stomach corpus, this model of progression from stem cells has been supported by studies in mice and human beings, showing abundant proliferation in the isthmus and clonal expansion of mutated cells from the stem cell region. An alternative theory proposes that gastric metaplasia arises from mature differentiated chief cells...
July 2017: Cellular and Molecular Gastroenterology and Hepatology
https://www.readbyqxmd.com/read/28560292/metaplasia-in-the-stomach-arises-from-gastric-chief-cells
#17
Jason C Mills, James R Goldenring
The development of intestinal-type gastric cancer is preceded by loss of parietal cells (oxyntic atrophy) and the induction of metaplastic cell lineages in the gastric mucosa. For example, mouse models have shown that spasmolytic polypeptide-expressing metaplasia can develop following oxyntic atrophy through transdifferentiation of zymogen-secreting chief cells. Evolution of spasmolytic polypeptide-expressing metaplasia from chief cells occurs via a coordinated dismantling of their secretory apparatus and reprogramming of their transcriptome...
July 2017: Cellular and Molecular Gastroenterology and Hepatology
https://www.readbyqxmd.com/read/28560291/gastrin-and-gastric-cancer
#18
REVIEW
Jill P Smith, Sandeep Nadella, Nick Osborne
Gastric cancer is the third leading cause of cancer-related mortality worldwide. Despite progress in understanding its development, challenges with treatment remain. Gastrin, a peptide hormone, is trophic for normal gastrointestinal epithelium. Gastrin also has been shown to play an important role in the stimulation of growth of several gastrointestinal cancers including gastric cancer. We sought to review the role of gastrin and its pathway in gastric cancer and its potential as a therapeutic target in the management of gastric cancer...
July 2017: Cellular and Molecular Gastroenterology and Hepatology
https://www.readbyqxmd.com/read/28560290/farnesoid-x-receptor-agonist-treatment-alters-bile-acid-metabolism-but%C3%A2-exacerbates-liver-damage-in-a-piglet-model-of-short-bowel%C3%A2-syndrome
#19
Prue M Pereira-Fantini, Susan Lapthorne, Cormac G M Gahan, Susan A Joyce, Jenny Charles, Peter J Fuller, Julie E Bines
BACKGROUND & AIMS: Options for the prevention of short-bowel syndrome-associated liver disease (SBS-ALDs) are limited and often ineffective. The farnesoid X receptor (FXR) is a newly emerging pharmaceutical target and FXR agonists have been shown to ameliorate cholestasis and metabolic disorders. The aim of this study was to assess the efficacy of obeticholic acid (OCA) treatment in preventing SBS-ALDs. METHODS: Piglets underwent 75% small-bowel resection (SBS) or sham surgery (sham) and were assigned to either a daily dose of OCA (2...
July 2017: Cellular and Molecular Gastroenterology and Hepatology
https://www.readbyqxmd.com/read/28560289/initiation-and-maintenance-of-gastric-cancer-a-focus-on-cd44-variant-isoforms-and-cancer-stem-cells
#20
REVIEW
Yana Zavros
Gastric cancer is the third most common cause of cancer-related death. Although the incidence of gastric cancer in the United States is relatively low, it remains significantly higher in some countries, including Japan and Korea. Interactions between cancer stem cells and the tumor microenvironment can have a substantial impact on tumor characteristics and contribute to heterogeneity. The mechanisms responsible for maintaining malignant cancer stem cells within the tumor microenvironment in human gastric cancer are largely unknown...
July 2017: Cellular and Molecular Gastroenterology and Hepatology
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