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Helicobacter pylori is a spiral, Gram-negative bacterium colonizing the gastric mucosa. Infection with this microorganism contributes to the morphological and physiological changes of stomach what is associated with the expression of numerous virulence factors. Their production allows H. pylori to avoid a response from the host immune system and facilitates chronic mucosal infection. Moreover, virulence factors have a destructive impact on eukaryotic cells and increase the amount of proinflammatory cytokines. Chronic inflammation may affect gastric secretion abilities by alterations in hormone levels, the amount of neuropeptide producing cells and the number of receptors for these compounds. It is also suggested that H. pylori can modulate activity of the endocrine system via molecular mimicry mechanism. The structural homology between antigens of this bacterium and neuropeptides contributes to the development of autoantibodies capable of suppressing the activity of hormones. Based on literature data, H. pylori is believed to affect not only the morphology and function of the stomach but also the physiology of human extragastric systems, including the endocrine system.
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Paweł Krzyżek (2017) studied this question.
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