Concurrent enteric helminth infection modulates inflammation and gastric immune responses and reduces helicobacter-induced gastric atrophy

Helicobacter pylori is causally associated with gastritis and gastric cance r. Some developing countries with a high prevalence of infection have high gastric cancer rates, whereas in others, these rates are low. The progressi on of helicobacter-induced gastritis and gastric atrophy mediated by type 1 T-helper cells may be modulated by concurrent parasitic infection. Here, i n mice with concurrent helminth infection, helicobacter-associated gastric atrophy was reduced considerably despite chronic inflammation and high heli cobacter colonization. This correlated with a substantial reduction in mRNA for cytokines and chemokines associated with a gastric inflammatory respon se of type 1 T-helper cells. Thus, concurrent enteric helminth infection ca n attenuate gastric atrophy, a premalignant lesion.