l'd like to know, that if IgA can be triggered against H. pylori infection, is it protective?
The presence in the serum of antibodies to H. pylori is suugestive of the presence of the bacterium only before a treatment. After eradication they have a slow decrease and cannot be used for detecting the disappearance of the organism. At the best of my knowledge, no anti-Hp antibody has a protective role against infection. In fact, IgA high levels may be detected in the serum of infected patients. Moreover, bacterial antigens may induce cross reaction eother in the stomach (see reation to parietal cell) and in other districts (see spermatozoa flagella). Finally, serum antibodies detection has only a screening value, but is not diagnostic.
Gastric mucus is turned over continuously and given the acidic environment and the relatively short time period in which IgA would be present, I don't believe it plays much of a role in conferring protection. H. pylori's ability to live within the gastric mucus layer, which can range in pH from 2.5-6 depending on the proximity to the gastric epithelial cells would seem to limit the effectiveness of any targeted antibody. I'm not certain as to the binding capacity of antibodies under severely acid conditions, but my guess would be their ability to bind antigen would most likely be compromised.
If IgA does successfully interact with Helicobacter at all, then it would presumably only bind successfully to bacteria within close proximity to the gastric epithelial cells (at a more neutral pH). While adherence has often been shown to be important for colonization, it has been hypothesized that only about 10% of a given bacterial population is needed to successfully adhere to the gastric epithelium in order to provide enough inflammation (and thereby nourishment) for the rest of the population to thrive.
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