Pathogenesis of<i>Helicobacter pylori</i>Infection

Maeda, Shin; Mentis, Αndreas

doi:10.1111/j.1523-5378.2007.00529.x

Cited by 49 publications

(37 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The pathogenesis of H. pylori infection is complex, and additional pathogenic factors, host factors, and their intramolecular cross talk continue to be discovered (18,(42)(43)(44)(45)(46)(47). Although H. pylori infection causes chronic gastric inflammation, the immune escape of H. pylori infection, particularly under high levels of IFN-g, has been less commonly reported.…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori Infection Activates Src Homology-2 Domain–Containing Phosphatase 2 To Suppress IFN-γ Signaling

Wang

Chen

Sheu

et al. 2014

The Journal of Immunology

View full text Add to dashboard Cite

Helicobacter pylori infection not only induces gastric inflammation but also increases the risk of gastric tumorigenesis. IFN-γ has antimicrobial effects; however, H. pylori infection elevates IFN-γ–mediated gastric inflammation and may suppress IFN-γ signaling as a strategy to avoid immune destruction through an as-yet-unknown mechanism. This study was aimed at investigating the mechanism of H. pylori–induced IFN-γ resistance. Postinfection of viable H. pylori decreased IFN-γ–activated signal transducers and activators of transcription 1 and IFN regulatory factor 1 not only in human gastric epithelial MKN45 and AZ-521 but also in human monocytic U937 cells. H. pylori caused an increase in the C-terminal tyrosine phosphorylation of Src homology-2 domain–containing phosphatase (SHP) 2. Pharmacologically and genetically inhibiting SHP2 reversed H. pylori–induced IFN-γ resistance. In contrast to a clinically isolated H. pylori strain HP238, the cytotoxin-associated gene A (CagA) isogenic mutant strain HP238CagAm failed to induce IFN-γ resistance, indicating that CagA regulates this effect. Notably, HP238 and HP238CagAm differently caused SHP2 phosphorylation; however, imaging and biochemical analyses demonstrated CagA-mediated membrane-associated binding with phosphorylated SHP2. CagA-independent generation of reactive oxygen species (ROS) contributed to H. pylori–induced SHP2 phosphorylation; however, ROS/SHP2 mediated IFN-γ resistance in a CagA-regulated manner. This finding not only provides an alternative mechanism for how CagA and ROS coregulate SHP2 activation but may also explain their roles in H. pylori–induced IFN-γ resistance.

show abstract

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori Infection Activates Src Homology-2 Domain–Containing Phosphatase 2 To Suppress IFN-γ Signaling

Wang

Chen

Sheu

et al. 2014

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…H. pylori also induces apoptosis of eukaryotic cells through bacterial molecules, such as vacuolating cytotoxin A (Vac A) (Yahiro et al, 1997;Gebert et al, 2003) and CagA, which is encoded by the cytotoxin-associated gene A. These virulence factors, along with host genetic and environmental factors, constitute a complex network to regulate chronic gastric injury and infl ammation, which is involved in a multistep process leading to gastric carcinogenesis (Isomoto et al, 2010;Maeda and Mentis, 2007). Other bacteria, such as the mycoplasmas that cause pneumonia, arthritis and infertility, usually exist in human respiratory, alimentary and genital tracts and they are surface epithelial parasites requiring exogenous cholesterol for membrane stability and cell entry (Metz and Kraft, 2010;Roediger, 2004;Hartmann, 2009).…”

Section: Introductionmentioning

confidence: 99%

Mycoplasma hyorhinis and Mycoplasma fermentans induce cell apoptosis and changes in gene expression profiles of 32D cells

Liu

Shou

2011

Biol. Res.

View full text Add to dashboard Cite

Infection of mycoplasmas has been linked to various human diseases including arthritis, pneumonia, infertility and cancer. While Mycoplasma hyorhinis and Mycoplasma fermentans have been detected in gastric adenocarcinomas, the mechanisms underlyine the pathogenesis are unknown. In this study, cell growth kinetics, Hoechst 33258 staining, DNA ladder assays, Western blotting analysis and cDNA microarray assays were performed to investigate the roles of M. hyorhinis and M. fermentans during infection of mammalian cells. Our data demonstrated that these mycoplasmas inhibid the growth of immortalised cell lines (32D and COS-7) ane tumor cell lines (HeLa and AGS). In addition, the infection of the 32D cell line with M. hyorhinis and M. fermentans induced compression of the nucleus, degradation of the cell genome and dysregulation of the expression of genes related to proliferation, apoptosis, tumorigenesis, signaling pathway and metabolism. Apoptosis related proteins Bcl-2, Bid and p53 were down-regulated, Fas was up-regulated and Bax was dysregulated in mycoplasma-infected 32D cells. Together, our data demonstrated that infection of mycoplasmas inhibitd cele growts through modifi cation of gene expression profi les and post-translation modifi cation of proliferation and apoptosis related proteins.

show abstract

“…[11][12][13][14] H. pylori infection is so common and as many as 50% of the world population is infected with, 15 and a good mean of detection, with the best combination of simplicity, sensitivity, specificity, cost-effectiveness and rapid accurate results, is necessary to guarantee the correct treatment and preventing unnecessary further investigations for these patients or those with negative H. pylori gastric diseases. This guided us to look for an optimization of the widely used rapid urease test that combines all the characteristics to be an excellent confidential cheap and widely available test for the detection of H. pylori.…”

Section: Discussionmentioning

confidence: 99%

Prospective study to evaluate the number and the location of biopsies in rapid urease test for diagnosis of Helicobacter Pylori

Rached

Saba

Yaghi³

et al. 2017

Gastroenterol Insights

View full text Add to dashboard Cite

Helicobacter pylori (H. pylori) can cause a wide variety of illnesses such as peptic ulcer disease, gastric adenocarcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma. The diagnosis and eradication of H. pylori are crucial. The diagnosis of H. pylori is usually based on the rapid urease test (RUT) and gastric antral biopsy for histology. The aim of this study is to evaluate the numbers of needed biopsies and their location (antrum/fundus) to obtain optimal result for the diagnosis of H. pylori. Three hundred fifty consecutive patients were recruited, 210 fulfill the inclusion criteria and had nine gastric biopsies for the detection of H. pylori infection: two antral for the first RUT (RUT1), one antral and one fundic for the second (RUT2), one antral for the third (RUT3) and two antral with two fundic for histology (HES, Giemsa, PAS). The reading of the 3 types of RUT was performed at 1 hour, 3 hours and 24 hours and biopsies were read by two experienced pathologists not informed about the result of RUT. Results of RUT were considered positive if H. pylori was found on histology of at least one biopsy. The RUT1 at 1h, 3h and 24h has a sensitivity of 72%, 82% and 89% and a specificity of 100%, 99% and 87% respectively. The positive predictive value (PPV) was 100%, 99% and 85% respectively and the negative predictive value (NPV) of 81%, 87% and 90%. The RUT2 at 1h, 3h and 24h, respectively, had a sensitivity of 86%, 87% and 91% and a specificity of 99%, 97% and 90%. The PPV was 99%, 96% and 88% and NPV of 89%, 90%, 94%. The RUT3 at 1h, 3h and 24h, respectively, had a sensitivity of 70%, 74% and 84% and a specificity of 99%, 99% and 94%. The PPV was 99%, 99% and 92% and NPV of 79%, 81% and 87%. The best sensitivity and specificity were obtained for RUT1 read at 3h, for RUT2 read 1h and 3h, and the RUT3 read at 24h.This study demonstrates that the best sensitivity and specificity of rapid test for urease is obtained when fundic plus antral biopsy specimens are used with a reading time at 3 hours.

show abstract

Pathogenesis ofHelicobacter pyloriInfection

Cited by 49 publications

References 52 publications

Helicobacter pylori Infection Activates Src Homology-2 Domain–Containing Phosphatase 2 To Suppress IFN-γ Signaling

Helicobacter pylori Infection Activates Src Homology-2 Domain–Containing Phosphatase 2 To Suppress IFN-γ Signaling

Mycoplasma hyorhinis and Mycoplasma fermentans induce cell apoptosis and changes in gene expression profiles of 32D cells

Prospective study to evaluate the number and the location of biopsies in rapid urease test for diagnosis of Helicobacter Pylori

Contact Info

Product

Resources

About