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Human Helicobacter pylori cytotoxin-associated gene A protein IgG,HP-CagA-IgG ELISA Kit
For research use only. Not for use in diagnostic procedures.For general protocol and instruction, please click the following links:Quantitative Elisa Kit InstructionSandwich ELISA kit general instruction Competition ELISA kit general instruction
Data sheet
| Assay time | 90 min |
| Assay Range | Qualitative Positive; Negative control, Cut-off Calibrator |
| Background | Helicobacter pylori is a spiral bacterium cultured from human gastric mucosa by Marshall in 1982. Studies have indicated that the presence of H. pylori is associated with a variety of gastrointestinal diseases including gastritis, duodenal and gastric ulcer, non-ulcer dyspepsia, gastric adenocarcinoma and lymphoma. The organism is present in 95-98% of patients with duodenal ulcer and 60-90% of patients with gastric ulcers. The studies have also demonstrated that removal of the organism by antimicrobial therapy is correlated with the resolution of symptoms and cure of diseases. Patients who present with clinical symptoms relating to the gastrointestinal tract can be diagnosed for H. pylori infection by two methods: 1) invasive techniques include biopsy followed by culture or histologic examination of biopsy specimen or direct detection of urease activity. 2) non-invasive techniques include urea breath tests and serological methods. All of the testing performed on biopsy samples are subject to errors related to sampling and interference of contaminated bacteria. H. pylori IgG, testing the presence of H. pylori specific IgG antibody is the technique of choice for serologic tests because of its accuracy and simplicity. Both the possession of the cytotoxin-associated gene A (CagA), and the production of a vacuolating cytotoxin encoded by the vacuolating cytotoxin A (VacA) gene, are linked to increased pathogenicity of H pylori strains. There is substantial evidence that H pylori infection, especially with the strains expressing the 128 kDa CagA protein, is associated with enhanced gastric inflammatory response and increased risk of developing atrophic gastritis, peptic ulcer and even GC. |
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