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Fecal metagenomics and metabolomics reveal gut microbial changes after bariatric surgery.
Yu D, Shu XO, Howard EF, Long J, English WJ, Flynn CR
(2020) Surg Obes Relat Dis 16: 1772-1782
MeSH Terms: Bariatric Surgery, Female, Gastric Bypass, Gastrointestinal Microbiome, Humans, Male, Metabolomics, Metagenomics, Middle Aged, Pilot Projects
Show Abstract · Added August 18, 2020
BACKGROUND - Evidence from longitudinal patient studies regarding gut microbial changes after bariatric surgery is limited.
OBJECTIVE - To examine intraindividual changes in fecal microbiome and metabolites among patients undergoing Roux-en-Y gastric bypass or vertical sleeve gastrectomy.
SETTING - Observational study.
METHODS - Twenty patients were enrolled and provided stool samples before and 1 week, 1 month, and/or 3 months after surgery. Shallow shotgun metagenomics and untargeted fecal metabolomics were performed. Zero-inflated generalized additive models and linear mixed models were applied to identify fecal microbiome and metabolites changes, with adjustment for potential confounders and correction for multiple testing.
RESULTS - We enrolled 16 women and 4 men, including 16 white and 4 black participants (median age = 45 years; presurgery body mass index = 47.7 kg/m). Ten patients had Roux-en-Y gastric bypass, 10 had vertical sleeve gastrectomy, and 14 patients provided postsurgery stool samples. Of 47 samples, median sequencing depth was 6.3 million reads and 1073 metabolites were identified. Microbiome alpha-diversity increased after surgery, especially at 3 months. Significant genus-level changes included increases in Odoribacter, Streptococcus, Anaerotruncus, Alistipes, Klebsiella, and Bifidobacterium, while decreases in Bacteroides, Coprocosccus, Dorea, and Faecalibacterium. Large increases in Streptococcus, Akkermansia, and Prevotella were observed at 3 months. Beta-diversity and fecal metabolites were also changed, including reduced caffeine metabolites, indoles, and butyrate.
CONCLUSIONS - Despite small sample size and missing repeated samples in some participants, our pilot study showed significant postsurgery changes in fecal microbiome and metabolites among bariatric surgery patients. Future large-scale, longitudinal studies are warranted to investigate gut microbial changes and their associations with metabolic outcomes after bariatric surgery.
Copyright © 2020 American Society for Bariatric Surgery. Published by Elsevier Inc. All rights reserved.
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10 MeSH Terms
Bacterial CagA protein compromises tumor suppressor mechanisms in gastric epithelial cells.
Palrasu M, Zaika E, El-Rifai W, Garcia-Buitrago M, Piazuelo MB, Wilson KT, Peek RM, Zaika AI
(2020) J Clin Invest 130: 2422-2434
MeSH Terms: Antigens, Bacterial, Apoptosis Regulatory Proteins, Bacterial Proteins, Epithelial Cells, Gastric Mucosa, HCT116 Cells, Helicobacter pylori, Humans, Neoplasm Proteins, Proteolysis, Stomach Neoplasms, Ubiquitination, X-Linked Inhibitor of Apoptosis Protein
Show Abstract · Added April 7, 2020
Approximately half of the world's population is infected with the stomach pathogen Helicobacter pylori. Infection with H. pylori is the main risk factor for distal gastric cancer. Bacterial virulence factors, such as the oncoprotein CagA, augment cancer risk. Yet despite high infection rates, only a fraction of H. pylori-infected individuals develop gastric cancer. This raises the question of defining the specific host and bacterial factors responsible for gastric tumorigenesis. To investigate the tumorigenic determinants, we analyzed gastric tissues from human subjects and animals infected with H. pylori bacteria harboring different CagA status. For laboratory studies, well-defined H. pylori strain B128 and its cancerogenic derivative strain 7.13, as well as various bacterial isogenic mutants were employed. We found that H. pylori compromises key tumor suppressor mechanisms: the host stress and apoptotic responses. Our studies showed that CagA induces phosphorylation of XIAP E3 ubiquitin ligase, which enhances ubiquitination and proteasomal degradation of the host proapoptotic factor Siva1. This process is mediated by the PI3K/Akt pathway. Inhibition of Siva1 by H. pylori increases survival of human cells with damaged DNA. It occurs in a strain-specific manner and is associated with the ability to induce gastric tumor.
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13 MeSH Terms
Surveillance of Gastric Intestinal Metaplasia.
Shah SC, Gawron AJ, Li D
(2020) Am J Gastroenterol 115: 641-644
MeSH Terms: Cause of Death, Gastric Mucosa, Global Health, Humans, Morbidity, Patient Selection, Population Surveillance, Precancerous Conditions, Risk Assessment, Stomach Neoplasms, Survival Rate
Added March 3, 2020
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11 MeSH Terms
Spotlight: Gastric Intestinal Metaplasia.
Shah SC, Gupta S, Li D, Morgan D, Mustafa RA, Gawron AJ
(2020) Gastroenterology 158: 704
MeSH Terms: Algorithms, Biopsy, Endoscopy, Gastrointestinal, Gastric Mucosa, Helicobacter Infections, Helicobacter pylori, Humans, Metaplasia, Population Surveillance, Practice Guidelines as Topic, Precancerous Conditions, Risk Factors, Stomach Neoplasms
Added March 3, 2020
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13 MeSH Terms
Histologic Subtyping of Gastric Intestinal Metaplasia: Overview and Considerations for Clinical Practice.
Shah SC, Gawron AJ, Mustafa RA, Piazuelo MB
(2020) Gastroenterology 158: 745-750
MeSH Terms: Biopsy, Endoscopy, Gastrointestinal, Gastric Mucosa, Health Knowledge, Attitudes, Practice, Humans, Metaplasia, Population Surveillance, Precancerous Conditions, Stomach Neoplasms
Added March 3, 2020
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9 MeSH Terms
Advancing the Science in Gastric Pre-Neoplasia: Study Design Considerations.
Davitkov P, Altayar O, Shah SC, Gawron AJ, Mustafa RA, Sultan S, Morgan DR
(2020) Gastroenterology 158: 751-759
MeSH Terms: Biomedical Research, Biopsy, Endoscopy, Gastrointestinal, Gastric Mucosa, Humans, Incidence, Metaplasia, Population Surveillance, Precancerous Conditions, Prevalence, Research Design, Risk Factors, Stomach Neoplasms
Added March 3, 2020
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13 MeSH Terms
AGA Technical Review on Gastric Intestinal Metaplasia-Epidemiology and Risk Factors.
Altayar O, Davitkov P, Shah SC, Gawron AJ, Morgan DR, Turner K, Mustafa RA
(2020) Gastroenterology 158: 732-744.e16
MeSH Terms: Ethnic Groups, European Continental Ancestry Group, Gastric Mucosa, Helicobacter Infections, Helicobacter pylori, Humans, Metaplasia, Precancerous Conditions, Risk Factors, Stomach Neoplasms, United States
Added March 3, 2020
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AGA Technical Review on Gastric Intestinal Metaplasia-Natural History and Clinical Outcomes.
Gawron AJ, Shah SC, Altayar O, Davitkov P, Morgan D, Turner K, Mustafa RA
(2020) Gastroenterology 158: 705-731.e5
MeSH Terms: Biopsy, Disease Progression, Endoscopy, Gastrointestinal, Gastric Mucosa, Helicobacter Infections, Helicobacter pylori, Humans, Metaplasia, Population Surveillance, Precancerous Conditions, Prevalence, Risk Factors, Stomach Neoplasms, United States
Added March 3, 2020
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14 MeSH Terms
Targeted mobilization of Lrig1 gastric epithelial stem cell populations by a carcinogenic type IV secretion system.
Wroblewski LE, Choi E, Petersen C, Delgado AG, Piazuelo MB, Romero-Gallo J, Lantz TL, Zavros Y, Coffey RJ, Goldenring JR, Zemper AE, Peek RM
(2019) Proc Natl Acad Sci U S A 116: 19652-19658
MeSH Terms: Adenocarcinoma, Animals, Carcinogenesis, Disease Models, Animal, Epithelial Cells, Female, Gastric Mucosa, Gastritis, Helicobacter Infections, Helicobacter pylori, Humans, Male, Membrane Glycoproteins, Mice, Mice, Knockout, Nerve Tissue Proteins, Precancerous Conditions, Primary Cell Culture, Risk Factors, Stem Cells, Stomach, Stomach Neoplasms, Type IV Secretion Systems
Show Abstract · Added September 27, 2019
-induced gastritis is the strongest risk factor for gastric adenocarcinoma, a malignancy preceded by a series of well-defined histological stages, including metaplasia. One microbial constituent that augments cancer risk is the type 4 secretion system (T4SS), which translocates the oncoprotein CagA into host cells. Aberrant stem cell activation is linked to carcinogenesis, and Lrig1 (leucine-rich repeats and Ig-like domains 1) marks a distinct population of progenitor cells. We investigated whether microbial effectors with carcinogenic potential influence Lrig1 progenitor cells ex vivo and via lineage expansion within -infected gastric mucosa. Lineage tracing was induced in (Lrig1/YFP) mice that were uninfected or subsequently infected with or an isogenic mutant (nonfunctional T4SS). In contrast to infection with wild-type (WT) for 2 wk, infection for 8 wk resulted in significantly increased inflammation and proliferation in the corpus and antrum compared with uninfected or mice infected with the mutant. WT -infected mice harbored significantly higher numbers of Lrig1/YFP epithelial cells that coexpressed UEA1 (surface cell marker). The number of cells coexpressing intrinsic factor (chief cell marker), YFP (lineage marker), and GSII lectin (spasmolytic polypeptide-expressing metaplasia marker) were increased only by WT In human samples, Lrig1 expression was significantly increased in lesions with premalignant potential compared with normal mucosa or nonatrophic gastritis. In conclusion, chronic infection stimulates Lrig1-expressing progenitor cells in a -dependent manner, and these reprogrammed cells give rise to a full spectrum of differentiated cells.
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23 MeSH Terms
Resolution of Gastric Cancer-Promoting Inflammation: A Novel Strategy for Anti-cancer Therapy.
Piazuelo MB, Riechelmann RP, Wilson KT, Algood HMS
(2019) Curr Top Microbiol Immunol 421: 319-359
MeSH Terms: Cytokines, Gastric Mucosa, Helicobacter Infections, Helicobacter pylori, Humans, Inflammation, Stomach Neoplasms, Tumor Microenvironment
Show Abstract · Added June 6, 2019
The connection between inflammation and cancer was initially recognized by Rudolf Virchow in the nineteenth century. During the last decades, a large body of evidence has provided support to his hypothesis, and now inflammation is recognized as one of the hallmarks of cancer, both in etiopathogenesis and ongoing tumor growth. Infection with the pathogen Helicobacter pylori is the primary causal factor in 90% of gastric cancer (GC) cases. As we increase our understanding of how chronic inflammation develops in the stomach and contributes to carcinogenesis, there is increasing interest in targeting cancer-promoting inflammation as a strategy to treat GC. Moreover, once cancer develops and anti-cancer immune responses are suppressed, there is evidence of a substantial shift in the microenvironment and new targets for immune therapy emerge. In this chapter, we provide insight into inflammation-related factors, including T lymphocytes, macrophages, pro-inflammatory chemokines, and cytokines, which promote H. pylori-associated GC initiation and growth. While intervening with chronic inflammation is not a new practice in rheumatology or gastroenterology, this approach has not been fully explored for its potential to prevent carcinogenesis or to contribute to the treatment of GC. This review highlights current and possible strategies for therapeutic intervention including (i) targeting pro-inflammatory mediators, (ii) targeting growth factors and pathways involved in angiogenesis in the gastric tumor microenvironment, and (iii) enhancing anti-tumor immunity. In addition, we highlight a significant number of clinical trials and discuss the importance of individual tumor characterization toward offering personalized immune-related therapy.
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8 MeSH Terms