Concurrent parasitic infection may modify immune response to h pylori infection and incidence of the development of precancerous gastric atrophy

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Abstract​

GASTROENTEROLOGY 2000;119:611

Helicobacter pylori infection is now recognized to be a major acquired factor in the pathogenesis of non-cardia gastric cancer. The development of gastric cancer in subjects with H. pyloriinfection is closely associated with the development of atrophic gastritis. But a paradox in the association between H. pylori and cancer has been the low prevalence of gastric cancer in Africa despite the high prevalence of H. pyloriinfection: the so-called African enigma.
Fox et al., noting that parasitic infection is common in the African population, investigated the possibility that concurrent parasitic infection might alter the immune response to H. pyloriinfection and reduce the incidence of atrophic gastritis. They postulated that a Th2-like response stimulated by helminth infections might modulate the Th1-like immune response induced by H. pylori infection and thus modify the outcome of the latter. To investigate this, they studied the response to Helicobacter felis in mice with and without concurrent nematode parasitic infection with a strictly enteric life cycle.
Reporting in the May issue Nature Medicine, the researchers showed that the concurrent helminth infection was associated with a considerably reduced incidence of Helicobacter-associated gastric atrophy, despite chronic inflammation, and high Helicobactercolonization. They were also able to show that the helminth infection resulted in a substantial reduction in messenger RNA cytokines associated with a gastric inflammatory Th1-like immune response.
“The results demonstrated that concurrent helminth infection may modify the immune response to gastric Helicobacter infection and the incidence of the development of atrophy, which is a precancerous condition,” said Kenneth E. L. McColl, M.D., of the Western Infirmary in Glasgow, Scotland. McColl noted that it remains to be seen whether the same will hold true for humans infected with H. pylori infection.
The finding was in line with a hypothesis advanced by Joel Weinstock, M.D., of the University of Iowa. Weinstock, who has suggested that a declining number of parasites in developed countries may be contributing to an increase in autoimmune diseases, has focused his studies on inflammatory bowel disease. “This is the first publication I know of that addresses the issue of gastritis caused by H. pylori,” he said, “and it implies again that modern industrialized countries cleaning up their environment and eliminating the exposure to helminths may be part of the cause for the spread of gastritis in our communities.”
“That doesn't mean we want people to go back and live in filth, but if it turns out that this is an extremely important organism, it may mean that if we colonize children with the right helminth, we may be able to prevent these diseases later in life.”