CagA IgA
Enzyme Immunoassay for the quantitative determination of IgA antibodies to Helicobacter pylori cytotoxin associated gene A Antigen or CagA-Ag in sera/plasma. The product is intended for the follow-up of patients showing gastrointestinal pathologies referable to H.pylori infection.
Helicobacter pylori (Hp) is a Gram negative bacterium, firstly isolated in gastric mucosa by Marshall and Warren in 1983. Hp has been recognized to be the agent responsible of most of cases of gastric mucosal damage and to play a role in the evolution of gastric diseases to carcinoma.
Recently, virulent strains have been observed showing a high molecular weight cytotoxin, constituted by 87 KDa monomers causing the vacuolation of the epithelial cells (VacA toxin) and severe damages to the gastric mucosa.
A protein associated to VacA, produced in strains bearing the related gene and showing a molecular weight of 128 KDa has been also observed. This protein named CagA-Ag is immunogenic and stimulate the patient to produce specific antibodies, both of IgG and IgA classes.
Their reactivity in the patient is considered a clinical sign of presence of an highly virulent strain of H.pylori and, for IgA, of an acute ongoing infection.
Microplates are coated with Helicobacter pylori specific CagAAg synthetic antigen.
In the 1st incubation, the solid phase is treated with diluted samples and anti CagA-Ag IgA are captured, if present, by the antigens.
After washing out all the other components of the sample, in the 2nd incubation bound anti CagA-Ag IgA are detected by the addition of anti hIgA antibody, labeled with peroxidase (HRP). The enzyme captured on the solid phase, acting on the substrate/chromogen mixture, generates an optical signal that is proportional to the amount of anti CagA-Ag IgA antibodies present in the sample.
IgA in the sample may be quantitated by means of a standard curve calibrated in arbitrary units per milliliter (Uarb/ml) as no international standard is available.
Interferences due to the presence of IgG are blocked directly in the well by the addition of anti hIgG adsorbent.
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