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

Nat Med. 2000 May;6(5):536-42. doi: 10.1038/75015.


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

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antibodies, Bacterial / blood
  • Antibody Specificity
  • Chemokines / biosynthesis
  • Female
  • Gastritis / immunology*
  • Gastritis / microbiology
  • Gastritis / parasitology
  • Gastritis / physiopathology
  • Helicobacter Infections / complications
  • Helicobacter Infections / immunology*
  • Immunoglobulin E / blood
  • Immunoglobulin G / blood
  • Mice
  • Mice, Inbred C57BL
  • Nematospiroides dubius / immunology*
  • Strongylida Infections / complications
  • Strongylida Infections / immunology*
  • Th1 Cells / immunology


  • Antibodies, Bacterial
  • Chemokines
  • Immunoglobulin G
  • Immunoglobulin E