A5065687560- Helicobacter pylori-related gastroenterology studies
- Veterinary medicine and infectious diseases
- Gastric Cancer Management and Outcomes
- Gut microbiota and health
- Cytokine Signaling Pathways and Interactions
- Eosinophilic Esophagitis
- Galectins and Cancer Biology
- IL-33, ST2, and ILC Pathways
- Viral gastroenteritis research and epidemiology
- Mycobacterium research and diagnosis
- Clostridium difficile and Clostridium perfringens research
- Liver Disease Diagnosis and Treatment
- Gastrointestinal disorders and treatments
- Cancer Immunotherapy and Biomarkers
- Microscopic Colitis
- Immune Cell Function and Interaction
- Microbial Metabolites in Food Biotechnology
- Hepatitis B Virus Studies
- Gastroesophageal reflux and treatments
- Plant Virus Research Studies
- Gastrointestinal motility and disorders
- Escherichia coli research studies
- Digestive system and related health
- Inflammatory Bowel Disease
- Salmonella and Campylobacter epidemiology
Northwest A&F University
2025
Fuyang Normal University
2025
Jiangsu University
2025
Affiliated Hospital of Jiangsu University
2025
Massachusetts Institute of Technology
2014-2024
Hiroshima Cosmopolitan University
2023
University of Fukui
2011
Columbia University
2011
Biological E (India)
2007
University of Alberta
1992-2003
<h3>Objectives</h3> Gastric colonisation with intestinal flora (IF) has been shown to promote <i>Helicobacter pylori</i> (<i>Hp</i>)-associated gastric cancer. However, it is unknown if the mechanism involves specific or diverse microbiota secondary atrophy. <h3>Design</h3> Altered Schaedler9s (ASF) and <i>Hp</i> were correlated pathology, immune responses mRNA expression for proinflammatory cancer-related genes in germ-free (GF), monoassociated (m<i>Hp</i>), restricted ASF (rASF; 3...
Helicobacter hepaticus -infected Rag 2 -/- mice emulate many aspects of human inflammatory bowel disease, including the development colitis and colon cancer. To elucidate mechanisms inflammation-induced carcinogenesis, we undertook a comprehensive analysis histopathology, molecular damage, gene expression changes during disease progression in these mice. Infected developed severe hepatitis by 10 wk post-infection, progressing into carcinoma 20 with pronounced pathology cecum proximal marked...
Helicobacter hepaticus causes chronic hepatitis and liver cancer in mice. It is the prototype enterohepatic species a close relative of pylori , also recognized carcinogen. Here we report complete genome sequence H. ATCC51449. has circular chromosome 1,799,146 base pairs, predicted to encode 1,875 proteins. A total 938, 953, 821 proteins have orthologs pylori, Campylobacter jejuni both pathogens, respectively. lacks most known virulence factors, including adhesins, VacA cytotoxin, almost all...
In this study, two identical copies of a 23S-5S gene cluster, which are separately situated within the Helicobacter pylori UA802 chromosome, were cloned and sequenced. Comparison DNA sequence H. 23S rRNA with known sequences other bacterial genes indicated that closely related to those Campylobacter spp. therefore belong in proposed Proteobacteria subdivision. The 5'-terminal nucleotide T or A is close Pribnow box could be -10 region transcription promoter for gene, suggesting...
Abstract Colorectal cancer in humans results from sequential genetic changes intestinal epithelia commencing with inactivation of the APC tumor suppressor gene. Roles for host immunity epithelial tumorigenesis are poorly understood. It has been previously shown that CD4+CD25+ lymphocytes inhibit colitis-associated tumors Rag-deficient mice. Here we show addition ApcMin/+ mice reduces multiplicity adenomas. Interleukin-10 was required regulatory cells therapeutic effect. Recipients showed...
ABSTRACT Campylobacter jejuni is a leading cause of human enterocolitis and associated with postinfectious complications, including irritable bowel syndrome Guillain-Barré syndrome. However, the pathogenesis C. infection remains poorly understood. Paracellular pathways in intestinal epithelial cells are gated by intercellular junctions (tight adherens junctions), providing functional barrier between luminal microbes host immune lamina propria. Here we describe alterations tight monolayers...
Abstract Inflammation associated with bacterial infections is a risk factor for cancers in humans, yet its role breast cancer remains poorly understood. We have previously shown that innate immune inflammatory response against intestinal bacteria sufficient to induce colon cancer. Here we report infecting Rag2-deficient C57BL/6 ApcMin/+ mice an pathogen, Helicobacter hepaticus, significantly promotes mammary carcinoma females and enhances adenoma multiplicity by tumor necrosis α...
Campylobacter jejuni continues to be a leading cause of bacterial enteritis in humans. However, because there are no readily available animal models study the pathogenesis C. jejuni-related diseases, significance potential virulence factors, such as cytolethal distending toxin (CDT), vivo poorly understood. Mice deficient NF-kappaB subunits (p50(-/-) p65(+/-)) C57BL/129 background particularly susceptible colitis induced by another enterohepatic microaerobe, Helicobacter hepaticus, which,...
Recombinase-activating gene-2-deficient (Rag2(-/-)) mice lacking functional lymphocytes provide a useful model of chronic inflammatory bowel disease-emulating events in human colon cancer. Infection Rag2(-/-) with Helicobacter hepaticus led to accumulation macrophages and neutrophils the colon, process temporally related up-regulation tissue inducible nitric oxide synthase (iNOS) expression at site infection increased (NO) production, as evidenced by urinary excretion nitrate. Progressive...
Bacterial cytolethal distending toxins (CDTs) containing DNase I-like activity can induce limited host DNA damage that leads to activation of the DNA-damage repair responses in cultured cell lines. However, vivo experimental evidence linking CDTs carcinogenesis is lacking. In this study, infection A/JCr mice with an isogenic mutant Helicobacter hepaticus lacking CDT (CDT mutant) induced chronic hepatitis comparable wild-type H. (Hh) at both 4 and 10 months post inoculation (MPI); however,...
The recently identified type VI secretion system (T6SS) of proteobacteria has been shown to promote pathogenicity, competitive advantage over competing microorganisms, and adaptation environmental perturbation. By detailed phenotypic characterization loss-of-function mutants, in silico, vitro vivo analyses, we provide evidence that the enteric pathogen, Campylobacter jejuni, possesses a functional T6SS exerts pleiotropic effects on two crucial processes – survival bile salt, deoxycholic acid...
Helicobacter pylori (H. pylori) delivers oncoprotein CagA into gastric epithelial cells via the T4SS and drives activation of multiple oncogenic signalling pathways. YAP, a core effector Hippo tumour suppressor pathway, is frequently overexpressed in human cancers, suggesting its potential tumor-promoting role. Although casual factor H. induced carcinogenesis, link between YAP pathway has not been identified. In this work, we investigated regulation by CagA.Expression E-cadherin protein...
// Jessica R. Lakritz 1 , Theofilos Poutahidis 1, 2 Sheyla Mirabal Bernard J. Varian Tatiana Levkovich Yassin M. Ibrahim Jerrold Ward 3 Ellen C. Teng Brett Fisher Nicola Parry Stephanie Lesage Natalie Alberg Sravya Gourishetti James G. Fox Zhongming Ge Susan E. Erdman Division of Comparative Medicine, Massachusetts Institute Technology, Cambridge, MA 02139, USA Laboratory Pathology, Faculty Veterinary Aristotle University Thessaloniki, Greece 54124 Global VetPathology, Montgomery Village, MD...
H. pylori infection is the strongest known risk factor for gastric carcinoma. The activation of yes-associated protein 1 (YAP) and β-catenin pathways has been associated with multiple tumor types. In this study, we investigated crosstalk between YAP in pylori-associated tumorigenesis. Immunohistochemical analysis expression was performed human cancer tissues. small molecules Super-TDU KYA1797K, pharmacological inhibitors β-catenin, respectively, were used to investigate role these signaling...
Helicobacter pylori (H. pylori) infection is the main risk for gastric cancer (GC). However, cellular heterogeneity and underlying molecular mechanisms in H. pylori-driven tumorigenesis are poorly understood.
Clinical and experimental evidence has demonstrated the potential role of probiotics in prevention or treatment inflammatory bowel disease. Probiotic clones with direct immunomodulatory activity may have anti-inflammatory effects intestine. We investigated roles tumor necrosis factor alpha (TNF-alpha)-inhibitory Lactobacillus a pathogen-induced murine colitis model. Murine-derived probiotic lactobacilli were selected vitro for their ability to inhibit TNF-alpha secretion by Helicobacter...
ABSTRACT The overall complexity of the microbial communities in gastrointestinal (GI) tracts mammals has hindered observations dynamics and interactions individual bacterial populations. However, such information is crucial for understanding diverse disease-causing protective roles that gut microbiota play their hosts. Here, we determine spatial distribution, interanimal variation, persistence bacteria most complex defined-flora (gnotobiotic) model system to date, viz., mice colonized with...
Helicobacter pylori infection results in chronic gastritis, which may progress to gastric cancer. In this study, we investigated the efficacy of H. eradication preventing progression gastritis cancer pylori-infected transgenic INS-GAS mice. induced severe dysplasia and classified as high-grade low-grade gastrointestinal intraepithelial neoplasia (GIN) mice at 28 weeks postinfection (WPI). therapy using omeprazole, metronidazole, clarithromycin was administered p.o. 8, 12, or 22 WPI. Compared...
Activities of CD4(+) regulatory (T(REG)) cells restore immune homeostasis during chronic inflammatory disorders. Roles for T(REG) in inflammation-associated cancers, however, are paradoxical. It is widely believed that function cancer mainly to suppress protective anticancer responses. However, we demonstrate here also reduce risk throughout the body by efficiently downregulating inflammation arising from gastrointestinal (GI) tract. Building on a "hygiene hypothesis" model which GI...