Dominant nonresponsiveness to Helicobacter pylori infection is associated with production of interleukin 10 but not gamma interferon.
Helicobacter pylori-induced gastritis is an essential precursor lesion for the development of peptic ulcers or gastric adenocarcinoma. We demonstrate that nonresponsiveness to H. pylori SS1 infection is dominantly inherited in mice. F(1) hybrid crosses between a nonresponder mouse and three responder strains all possessed the nonresponder phenotype. Secretion of interleukin-10 but not gamma interferon was associated with nonresponsiveness to infection.
Sutton
P
P
School of Microbiology and Immunology, University of New South Wales, Sydney, New South Wales 2052, Australia. P.Sutton@unsw.edu.au
Kolesnikow
T
T
Danon
S
S
Wilson
J
J
Lee
A
A
D000230:Adenocarcinoma / Q000209:etiology; D000818:Animals; D003433:Crosses, Genetic; D005756:Gastritis / Q000235:genetics*; D005799:Genes, Dominant; D016481:Helicobacter Infections / Q000235:genetics*; D016480:Helicobacter pylori; D007371:Interferon-gamma / Q000378:metabolism*; D016753:Interleukin-10 / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D008808:Mice, Inbred CBA; D010437:Peptic Ulcer / Q000209:etiology
D016753:Interleukin-10; D007371:Interferon-gamma