Sources of variation of Helicobacter pylori treatment success in adults worldwide: a meta-analysis

Fischbach, Lori; Goodman, Karen J.; Feldman, Mark; Aragaki, Corinne

doi:10.1093/ije/31.1.128

Cited by 107 publications

(157 citation statements)

References 44 publications

Supporting

Mentioning

147

Contrasting

Order By: Relevance

“…A triple-therapy regimen for 7 to 14 days is used as the first-line treatment for H. pylori-infected patients, but the failure rate is around 20 to 30% (7,9). The failure of antibiotic treatment has been assumed to be due to the selection of an antibiotic-resistant mutant.…”

Section: Vol 78 2010mentioning

confidence: 99%

Invasion and Multiplication of Helicobacter pylori in Gastric Epithelial Cells and Implications for Antibiotic Resistance

Chu¹,

Wang

et al. 2010

Infect Immun

View full text Add to dashboard Cite

Helicobacter pylori is a Gram-negative, spiral-shaped bacterium that infects more than 50% of the human population and can cause gastritis, peptic ulcer, or gastric malignancies. It is generally viewed as an extracellular microorganism. In a gentamicin protection assay on AGS or MKN45 cells, H. pylori could invade the epithelial cells and multiply within double-layer vesicles either on the plasma membrane or in the cytoplasm. A 5-fold increase in the number of bacteria was recultured from the infected cells at 12 h, compared with the number of invading cells at 2.5 h postinfection. The autophagic vesicles induced by H. pylori are the sites of replication and also of the degradation of the replicating bacteria after fusion with lysosomes. Many H. pylori bacteria in coccoid form associated with the plasma membrane can be released into culture. Only cellpenetrating antibiotics can enhance the intracellular killing of the replicating bacteria. The multiplication of H. pylori within cells provides a niche for its resistance to antibacterial therapy and has a significant impact on its biological life cycle.Helicobacter pylori is a Gram-negative, flagellated, microaerophilic bacterium that selectively colonizes the gastric mucosa. It infects people worldwide and is correlated with socioeconomic conditions (24). The prevalence among middleaged adults is over 80% in many developing countries. Overt disease, however, occurs in only 10 to 20% of infected individuals. The most common pathology associated with H. pylori infection is chronic active gastritis and peptic ulceration. A long-term chronic infection will increase the risk of gastric adenocarcinoma and mucosa-associated lymphoid-tissue lymphoma (19). Gastric mucosa is well protected against bacterial infections. However, H. pylori adapts and resides in the mucus and achieves attachment to epithelial cells, evasion of the immune responses, and persistent colonization in the stomach. It is not well understood why the immune system fails to clear H. pylori infection. Furthermore, the mechanisms controlling the induction and maintenance of the H. pylori-induced chronic inflammation are only partly understood.Although H. pylori is generally viewed as a noninvasive pathogen, a number of in vivo and in vitro studies have shown that H. pylori is invasive, and it can reside in the vacuole in the cytoplasm or even replicate on the cell membrane to form a microcolony (2,11,25). This suggests that H. pylori can be considered a facultative intracellular organism (6, 20). We have reported that H. pylori can multiply in macrophages and bone marrow-derived dendritic cells with autophagy induction (27,28). In this study, we further extended this line of research to epithelial cells and found that H. pylori could invade and replicate in epithelial cells. Thus, H. pylori can be considered an intracellular microorganism, and this has an impact on its own biological life cycle and its resistance to antibiotics. MATERIALS AND METHODSBacterial strains and culture. The H. pylori clinical i...

show abstract

Section: Vol 78 2010mentioning

confidence: 99%

Invasion and Multiplication of Helicobacter pylori in Gastric Epithelial Cells and Implications for Antibiotic Resistance

Chu¹,

Wang

et al. 2010

Infect Immun

View full text Add to dashboard Cite

show abstract

“…3 Although increased antimicrobial resistance has been seen with each of the agents used in treatment of H. pylori, the increase in treatment failure can be attributed in large part to resistance to clarithromycin. [4][5][6] It has been previously demonstrated that point mutations in domain V of the 23S rRNA gene are responsible for the resistance of H. pylori to macrolides, 7 with the three major point mutations being A2142G, A2143G, and A2142C. 7 The most frequent of these are transitions of adenine to guanine at the 2143 or 2142 positions, which account for 480% of clarithromycin resistance seen worldwide and B90% of resistance seen in developed countries.…”

mentioning

confidence: 99%

PCR detection of clarithromycin-susceptible and -resistant Helicobacter pylori from formalin-fixed, paraffin-embedded gastric biopsies

et al. 2013

View full text Add to dashboard Cite

Antimicrobial resistance to clarithromycin is a growing concern in the treatment of Helicobacter pylori and is associated with three major point mutations of the 23S rRNA, A2142C, A2142G, and A2143G. The use of traditional culture-based methods for determination of clarithromycin resistance in H. pylori are time consuming and lack sensitivity. We implemented a real-time PCR with melt curve analysis to detect and characterize H. pylori in formalin-fixed, paraffin-embedded gastric biopsy specimens to assess the frequency of clarithromycin resistance mutations in our study population. One hundred and fifty-three formalin-fixed, paraffin-embedded gastric biopsies were chosen on the basis of positive immunohistochemical staining for H. pylori and an accompanying histopathological diagnosis of Helicobacter-associated gastritis. New adjacent sections were taken for immunohistochemical staining and DNA extraction with subsequent testing by PCR assay and melt curve analysis using a primer and probe combination first described by Oleastro et al. 12 One hundred and forty-six samples demonstrated adequate amplification of a human DNA control target. Of these, there were 122 H. pylori immunohistochemistry-positive samples. In all, 103 out of 122 (84%) immunohistochemistry-positive samples demonstrated amplifiable H. pylori 23S rRNA gene target and 19 (16%) demonstrated no amplification of H. pylori. Twenty-two samples were negative for H. pylori by immunohistochemistry and PCR. Two were negative for H. pylori by immunohistochemistry, but were positive for H. pylori by PCR. In all, 52 out of 105 (50%) PCR-positive samples demonstrated resistance mutations, and it was determined that a heterogeneous population of mutated and unmutated organisms was present in 11 out of 52 samples. The use of PCR assays allows for a timely assessment of clarithromycin resistance status without the disadvantages of culture-based methods, and may lead to a decrease in treatment failure rates.

show abstract

“…This distinction has caused considerable confusion since gastritis is often used to describe endoscopic or radiologic characteristics of the gastric mucosa rather than specific histologic findings. Epithelial cell damage and regeneration without associated inflammation is referred to as "gastropathy" [63,64].…”

Section: Review Of Literaturementioning

confidence: 99%

“…Acute ("active") inflammation is usually associated with neutrophilic infiltration, while chronic inflammation is usually characterized by mononuclear cells, chiefly lymphocytes, plasma cells and macrophages. A practical clinicopathologic framework for the classification of gastritis and gastropathy based upon these factors can be proposed [63].…”

Section: Review Of Literaturementioning

confidence: 99%

The Study of Association between Helicobacter pylori (H. pylori) and Chronic Obstructive Pulmonary Disease (COPD)

Deerpaul¹

2014

J Pulm Respir Med

View full text Add to dashboard Cite

Sources of variation of Helicobacter pylori treatment success in adults worldwide: a meta-analysis

Abstract: More effective treatments are needed for most populations of the world where H. pylori infection in children and drug resistance are common. Current treatment guidelines do not coincide with the best treatment regimens identified in this meta-analysis.

Cited by 107 publications

References 44 publications

Invasion and Multiplication of Helicobacter pylori in Gastric Epithelial Cells and Implications for Antibiotic Resistance

Invasion and Multiplication of Helicobacter pylori in Gastric Epithelial Cells and Implications for Antibiotic Resistance

PCR detection of clarithromycin-susceptible and -resistant Helicobacter pylori from formalin-fixed, paraffin-embedded gastric biopsies

The Study of Association between Helicobacter pylori (H. pylori) and Chronic Obstructive Pulmonary Disease (COPD)

Contact Info

Product

Resources

About