Nature Medicine
6, 536 - 542 (2000)
doi:10.1038/75015
Concurrent enteric helminth infection modulates inflammation and gastric
immune responses and reduces helicobacter-induced gastric atrophyJames G. Fox1, Paul Beck3, Charles A. Dangler1, Mark T. Whary1, Timothy C. Wang3, Hai Ning Shi2
& Cathryn Nagler-Anderson21
Division of Comparative Medicine, Massachusetts Institute
of Technology Cambridge, Massachusetts, 02139,
USA
2
Mucosal Immunology Laboratory, Pediatric Gastroenterology,
Massachusetts General Hospital, Boston, Massachusetts
02114, USA
3
Gastroenterology Unit Department of Medicine, Massachusetts
General Hospital, Boston, Massachusetts 02114
, USA
Correspondence should be addressed to James G. Fox jgfox@mit.edu
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.
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