DNA Transfer and Toll-like Receptor Modulation by Helicobacter pylori

Varga, Matthew G.; Peek, Richard M.

doi:10.1007/978-3-319-50520-6_8

Cited by 30 publications

(37 citation statements)

References 137 publications

(205 reference statements)

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“…Thus, the pattern of the host's immune response beyond genetic and environmental factors is also essential for understanding the pathology of GC [59]. TLRs, a class of transmembrane receptors [60], play an important role in defense against Helicobacter pylori (H. pylori) widely known as a class I carcinogen in GC [60,61]. Therefore, the abnormal expression of TLRs is closely related to tumorigenesis and cancer progression and a better understanding of TLRs will provide new diagnostic or predictive markers for the diagnosis of GC.…”

Section: Discussionmentioning

confidence: 99%

Identification of Novel Hub Genes Associated With Gastric Cancer Using Integrated Bioinformatics Analysis

Zhang

Qiao

et al. 2020

Preprint

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Background: Gastric cancer (GC) is one of the most common solid malignant tumors worldwide with a high-recurrence-rate. Identifying the molecular signatures and specific biomarkers of GC might provide novel clues for GC prognosis and targeted therapy.Methods: Gene expression profiles were obtained from the ArrayExpress and Gene Expression Omnibus database. Differentially expressed genes (DEGs) were picked out by R software. The hub genes were screened by cytoHubba plugin. Their prognostic values were assessed by Kaplan–Meier survival analyses and the gene expression profiling interactive analysis (GEPIA). Finally, qRT-PCR in GC tissue samples was established to validate these DEGs. Results: Total of 295 DEGs were identified between GC and their corresponding normal adjacent tissue samples in E-MTAB-1440, GSE79973, GSE19826, GSE13911, GSE27342, GSE33335 and GSE56807 datasets, including 117 up-regulated and 178 down-regulated genes. Among them, 7 vital upregulated genes (HMMR, SPP1, FN1, CCNB1, CXCL8, MAD2L1 and CCNA2) were selected. Most of them had a significantly worse prognosis except SPP1. Using qRT-PCR, we validated that their transcriptions in our GC tumor tissue were upregulated except SPP1 and FN1, which correlated with tumor relapse and predicts poorer prognosis in GC patients.Discussion: We have identified 5 upregulated DEGs (HMMR, CCNB1, CXCL8, MAD2L1, and CCNA2) in GC patients with poor prognosis using integrated bioinformatical methods, which could be potential biomarkers and therapeutic targets for GC treatment.

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Section: Discussionmentioning

confidence: 99%

Identification of Novel Hub Genes Associated With Gastric Cancer Using Integrated Bioinformatics Analysis

Zhang

Qiao

et al. 2020

Preprint

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“…H. pylori is classified into two types according to the expression of cag pathogenicity island ( cag PAI)[ 1 ]. cag PAI is a gene locus necessary to assemble type IV secretion system (T4SS), a syringe and needle-like structure[ 1 , 31 ]. The primary function of T4SS, encoded by cag PAI, is the injection of pathogenic factors, such as cytotoxin-associated gene A (CagA) into the host gastric ECs upon attachment to the epithelium[ 1 , 31 ].…”

Section: Type IV Secretion System Of H Pylori Andmentioning

confidence: 99%

“…cag PAI is a gene locus necessary to assemble type IV secretion system (T4SS), a syringe and needle-like structure[ 1 , 31 ]. The primary function of T4SS, encoded by cag PAI, is the injection of pathogenic factors, such as cytotoxin-associated gene A (CagA) into the host gastric ECs upon attachment to the epithelium[ 1 , 31 ]. Thus, cag PAI-positive H. pylori can cause gastric mucosal injury through injection of CagA mediated by T4SS.…”

Section: Type IV Secretion System Of H Pylori Andmentioning

confidence: 99%

Nucleotide-binding oligomerization domain 1 andHelicobacter pyloriinfection: A review

Minaga

Watanabe

Kamata

et al. 2018

WJG

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Nucleotide-binding oligomerization domain 1 (NOD1) is an intracellular innate immune sensor for small molecules derived from bacterial cell components. NOD1 activation by its ligands leads to robust production of pro-inflammatory cytokines and chemokines by innate immune cells, thereby mediating mucosal host defense systems against microbes. Chronic gastric infection due to Helicobacter pylori (H. pylori) causes various upper gastrointestinal diseases, including atrophic gastritis, peptic ulcers, and gastric cancer. It is now generally accepted that detection of H. pylori by NOD1 expressed in gastric epithelial cells plays an indispensable role in mucosal host defense systems against this organism. Recent studies have revealed the molecular mechanism by which NOD1 activation caused by H. pylori infection is involved in the development of chronic gastritis and gastric cancer. In this review, we have discussed and summarized how sensing of H. pylori by NOD1 mediates the prevention of chronic gastritis and gastric cancer.

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“…TLR9 recognizes HSV-2 by plasmacytoid DCs through an endocytic pathway. 112 Moreover, it elicits innate immune responses against Aspergillus fumigatus, 113 Helicobacter pylori, 114 Plasmodium falciparum, 115 Toxoplasma gondii, 116 murine cytomegalovirus, and HSV-1. 23 DDX41 and AIM2 DNA sensors have been reported to induce phosphorylation of IRF3 and subsequent type I IFN responses in the RAW264.7 mouse macrophage cell line following recombinant adenoviral vector infection.…”

Section: A Antimicrobial Immunitymentioning

confidence: 99%

Sensing Self and Non-Self DNA by Innate Immune Receptors and Their Signaling Pathways

Sok¹,

Ori²,

Nagoor³

et al. 2018

Crit Rev Immunol

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The innate immune system serves as the first line of defense to protect the host from pathogen infection. As a first step, the pattern recognition receptors (PRRs) recognize pathogen-associated molecular patterns (PAMPs), such as non-self DNA derived from pathogens, and damage-associated molecular patterns (DAMPs), such as self DNA released from damaged or injured cells. Sensing of such DNAs elicits innate immune responses through the production of type I interferons (IFNs) and proinflammatory cytokines resulting from the activation of interferon regulatory factor 3 (IRF3) and nuclear factor kappa B (NF-κB), respectively. These cytokines are key players in interlinking innate and adaptive immune responses. However, defects in DNA sensors and their signaling cascades lead to dysregulation of immune responses, autoimmune diseases, and cancer progression. Here we provide an update on DNA signaling pathways in response to pathogen infection and cell injury, and on the roles of regulators in governing the immune system and maintaining host homeostasis. We also discuss the evasion of immunosurveillance by pathogens.

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DNA Transfer and Toll-like Receptor Modulation by Helicobacter pylori

Cited by 30 publications

References 137 publications

Identification of Novel Hub Genes Associated With Gastric Cancer Using Integrated Bioinformatics Analysis

Identification of Novel Hub Genes Associated With Gastric Cancer Using Integrated Bioinformatics Analysis

Nucleotide-binding oligomerization domain 1 andHelicobacter pyloriinfection: A review

Sensing Self and Non-Self DNA by Innate Immune Receptors and Their Signaling Pathways

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