Antibiotic Treatment of Helicobacter pylori Infection

Unge, Peter

doi:10.1007/978-3-642-60013-5_13

Cited by 10 publications

(9 citation statements)

References 63 publications

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“…Bacterial adhesion to host cells is an important initial event in the pathogenesis of gastric malignancies, and inhibition of bacterial adhesion may prevent certain pathogen-related diseases, such as DU and GC. The current eradication strategy requires a combination of 2 to 3 antibiotics and a proton pump inhibitor (39). As such, it is necessary to develop other therapeutic alternatives due to ever-increasing concerns about antibiotic resistance (40), the lack of protection against re-infection, the necessity of taking a long-term prescription for complete eradication, and the high cost of therapy.…”

Section: Discussionmentioning

confidence: 99%

Role for α- l -fucosidase in the control of Helicobacter pylori -infected gastric cancer cells

Liu

Huang

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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Infecting about one-half of the global human population, Helicobacter pylori is well established as the primary cause of gastritis, duodenal ulcer, and gastric cancer. Currently there is no clear information regarding if and how host cells interact with H. pylori, and if such interactions are dependent on the type of gastric disease. Using fluorescently labeled fucose-containing glycoconjugates, we provide evidence observing both the uptake of L-fucose from gastric cancer cells to H. pylori and that human ␣-L-fucosidase 2 (FUCA2) is secreted only under coculture conditions (i.e., host cells infected with H. pylori). Upon depletion of FUCA2 by RNA interference and detection of translocated CagA (a virulence factor of H. pylori) in host cells, FUCA2 was found to be essential for H. pylori adhesion, in particular to the gastric cancer-and duodenal ulcer-specific strains. Additionally FUCA2 was shown to significantly enhance the expression of Lewis x antigen in H. pylori, which is critical for bacterial cell adhesion in the pathogenesis and defense strategy to escape host surveillance. These findings not only demonstrate an important connection between FUCA2 and the adhesion, growth, and pathogenicity of H. pylori, but also support the idea that FUCA2 is a potential target for clinical diagnosis and therapeutic intervention of H. pylori-related diseases.

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Section: Discussionmentioning

confidence: 99%

Role for α- l -fucosidase in the control of Helicobacter pylori -infected gastric cancer cells

Liu

Huang

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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“…Therefore, successful eradication of H. pylori from infected populations is considered an important public health goal. The currently used eradication strategy focuses on treatment of those individuals that display overt disease symptoms with a combination of two to three antibiotics and a proton pump inhibitor (5). However, the increasing prevalence of antibiotic resistance (6), the lack of protection against reinfection, and the high cost limit the usefulness of this strategy for control of H. pylori-related diseases.…”

mentioning

confidence: 99%

Protective immunity against Helicobacter is characterized by a unique transcriptional signature

Mueller

O’Rourke

Chu

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

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Immunization with a whole-cell sonicate vaccine of Helicobacter felis in conjunction with cholera toxin as a mucosal adjuvant induces long-term protective immunity in a majority of laboratory mice. We have combined gene expression profiling and immunohistochemical analysis on a set of immunized animals to better understand the mechanism of protection. The stomachs of protected animals exhibited a strikingly different transcriptional profile compared with those of nonprotected or control mice, indicating that vaccination targets the appropriate site and leaves a molecular signature. Among the genes whose up-regulation is significantly correlated with protection are a number of adipocytespecific factors. These include the fat-cell-specific cytokines adipsin, resistin, and adiponectin and the adipocyte surface marker CD36. Interestingly, potentially protective T and B lymphocytes can be found embedded in the adipose tissue surrounding protected stomachs but never in control or unprotected stomachs. Adipsinspecific immunohistochemical staining of protected stomach sections further revealed molecular cross-talk between adjacent lymphoid and adipose cell populations. We propose a mechanism of protection that involves the effector responses of either or both lymphocyte subclasses as well as the previously unappreciated paracrine functions of adipose tissue surrounding the resident lymphocytes.rodent ͉ lymphocytes ͉ bacterial infections ͉ vaccination ͉ mucosa G astric infection with the bacterium Helicobacter pylori is associated with the development of acute chronic gastritis, peptic ulcer disease, and two gastric malignancies, adenocarcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma (1-4). Therefore, successful eradication of H. pylori from infected populations is considered an important public health goal. The currently used eradication strategy focuses on treatment of those individuals that display overt disease symptoms with a combination of two to three antibiotics and a proton pump inhibitor (5). However, the increasing prevalence of antibiotic resistance (6), the lack of protection against reinfection, and the high cost limit the usefulness of this strategy for control of H. pylori-related diseases. The development of a prophylactic vaccine with possible therapeutic applications is widely viewed as a promising complementary approach.The first animal model for Helicobacter infection became available in 1990 with the demonstration that Helicobacter felis could colonize the murine stomach and induce chronic active gastritis (7). Using this model, Chen et al. (8) were able to demonstrate that immunization with a whole-cell H. felis sonicate oral vaccine in combination with cholera toxin as a mucosal adjuvant can protect the host from later challenge with large viable doses of the same strain. Moreover, the organism load of an existing H. felis infection could also be significantly reduced with the same vaccine regimen, thereby demonstrating the effect of therapeutic immunization (9). Observations made b...

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“…It is important to use well-defined and validated combinations of drugs (61)(62)(63). There is no ideal therapy to eradicate the H. pylori infection (61,63,64), according to the review by Unge (61).…”

Section: Treatment Of H Pylori and Evaluation Of Therapeutic Efficacymentioning

confidence: 99%

“…There is no ideal therapy to eradicate the H. pylori infection (61,63,64), according to the review by Unge (61). The highest eradication rate (90%) for treatment of H. pylori infection was achieved with a drug combination using omeprazole 20 mg twice a day plus metronidazole 400 mg (or tinidazole 250-500 mg) twice a day, plus clarithromycin 250-500 mg twice a day for 7 days.…”

Section: Treatment Of H Pylori and Evaluation Of Therapeutic Efficacymentioning

confidence: 99%

Laboratory tests for the evaluation of Helicobacter pylori infections

Nakamura

2001

Clinical Laboratory Analysis

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Helicobacter pylori is a highly motile bacterium with multiple unipolar flagella, and it produces the urease enzyme. The flagella and urease are the virulence factors of H. pylori. H. pylori often establishes a chronic infection in the stomach that may lead to gastric and duodenal ulcers, gastric cancers, gastric lymphomas, and other gastrointestinal diseases. There are several different invasive and noninvasive clinical laboratory tests for H. pylori. Laboratory testing is not indicated in asymptomatic patients and should be considered only if treatment of H. pylori infection is planned. Invasive tests for H. pylori, such as tissue histology, culture, and rapid urease tests, are used if an endoscopy is performed on the patient. The noninvasive tests for H. pylori, such as enzyme antibody and urea breath tests, are recommended in patients whose symptoms do not warrant endoscopy. The urea breath test is very useful and is recommended to evaluate effectiveness in the eradication and treatment of H. pylori infections. Nucleic acid tests can complement other diagnostic procedures, and are useful in evaluating fixed biopsy tissue, environmental samples, gastric juices, oral secretions, and stool samples.

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Antibiotic Treatment of Helicobacter pylori Infection

Cited by 10 publications

References 63 publications

Role for α- l -fucosidase in the control of Helicobacter pylori -infected gastric cancer cells

Role for α- l -fucosidase in the control of Helicobacter pylori -infected gastric cancer cells

Protective immunity against Helicobacter is characterized by a unique transcriptional signature

Laboratory tests for the evaluation of Helicobacter pylori infections

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