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Helicobacter pylori IgG Control Serum BC118G



  • Virion/Serion Diagnostic Kit Control for research use (RUO)
  • Helicobacter pylori IgG Control Serum
  • Applications: ELISA
  • IgG control serum
  • Ready-to-use; pre-diluted for SERION ELISA classic and SERION ELISA antigen assays
  • 3 mL
Weight1 lbs
Dimensions9 × 5 × 2 in

Helicobacter pylori reactive IgG

species reactivity

Helicobacter pylori



assay type

Indirect & quantitative

available size

3 mL

Available product – Helicobacter pylori IgG Control Serum BC118G

Research area
Infectious Disease
Store at 2-8°C.
Associated products
Helicobacter pylori Antigen (BA118VS)
Helicobacter pylori IgA Control Serum (BC118A)
Helicobacter pylori IgG Control Serum (BC118G)
Helicobacter pylori IgM Control Serum (BC118M)
Helicobacter pylori IgA ELISA Kit (ESR118A)
Helicobacter pylori IgG ELISA Kit (ESR118G)
Helicobacter pylori IgM ELISA Kit (ESR118M)
target relevance
Helicobacter pylori
Structure and strains
Helicobacter pylori, previously known as Campylobacter pylori, is a gram-negative, flagellated, helical bacterium. Mutants can have a rod or curved rod shape, and these are less effective. Its helical body (from which the genus name, Helicobacter, derives) is thought to have evolved in order to penetrate the mucous lining of the stomach, helped by its flagella, and thereby establish infection. The bacterium was first identified as the causal agent of gastric ulcers in 1983 by the Australian doctors Barry Marshall and Robin Warren.
More than 50% of the world's population harbor Helicobacter pylori in their upper gastrointestinal tract. As a consequence, infections with this spirally formed, gram-negative bacterium belong to the most frequently occuring chronic bacterial diseases.

80 to 90% of all gastritis cases are traceable to an Helicobacter pylori infection. The person-to-person transmission is still not fully elucidated, but oral-oral and faecal-oral route mechanisms are discussed. Diseases associated with H. pylori infections include Ulcus duodeni, Ulcus ventriculi, stomach cancer and the seldom occuring MALT (Mucosa Associated Lymphatic Tissue) lymphoma. Phenotypic differences between different Helicobacter pylori isolates are limited to their ability to express the vacuolating cytotoxin (VacA) and its associated gene products (cytotoxin-associated genes; CagA). Due to phenotypic differences Helicobacter pylori isolates can be divided into virulent (type I) and non-virulent (type II) strains. Patients suffering from peptic or duodenal ulcers are more frequently infected with VacA and CagA producing Helicobacter pylori type I strains. Diagnose I
Detection and diagnosis
In the diagnosis of H. pylori infections, a distinction is made between non-invasive and invasive methods. Invasive procedures contain histology, urease rapid test and microbiological techniques such as cultivation and PCR. The C13-breath test, the Helicobacter pylori antigen detection in stool samples and serological antibody detection based on ELISA or immunoblot belong to the group of non-invasive methods. The detection of serum antibodies can be used for therapy control after eradication therapy



Published literature highly relevant to the biological target of this product and referencing this antibody or clone are retrieved from PubMed database provided by The United States National Library of Medicine at the National Institutes of Health.



relevant to this product
BC118G protocol


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