Helicobacter pylori infection in wild-type and cytokine-deficient C57BL/6 and BALB/c mouse mutants.
Helicobacter pylori causes gastroduodenal ulcer disease in humans. T lymphocytes and their cytokines are thought to play a substantial role in the control of H. pylori infection. To determine the importance of T helper (Th) cytokines and background genes we investigated the natural course of H. pylori infection in BALB/c and C57BL/6 wild-type or mutant mice deficient for either interleukin (IL)-4 or interferon (IFN)-gamma. H. pylori SPM 326 persisted for at least six months in C57BL/6 but was cleared by BALB/c wild-type mice nine weeks postinfection. H. pylori was recovered more frequently from IFN-gamma(-/-) BALB/c and IFN-gamma( -/-) C57BL/6 mice than from the respective wild-type animals. In contrast, IL-4 deficiency had no detectable effect on H. pylori recovery rates from either strain of mice. Our data suggest a protective role of IFN-gamma by mediating inflammation in murine H. pylori infection. In addition, our data emphasize that background genes which differ between BALB/c and C57BL/6 mice regulate the clearance of H. pylori.
Kamradt
A E
AE
Max-Planck-Institut for Infection Biology, Department of Immunology, Monbijoustr. 2, 10117, Berlin, Germany.
Greiner
M
M
Ghiara
P
P
Kaufmann
S H
SH
D000818:Animals; D005260:Female; D016481:Helicobacter Infections / Q000276:immunology* / Q000382:microbiology* / Q000473:pathology; D016480:Helicobacter pylori / Q000254:growth & development / Q000302:isolation & purification*; D007371:Interferon-gamma / Q000172:deficiency / Q000235:genetics / Q000276:immunology / Q000502:physiology*; D015847:Interleukin-4 / Q000172:deficiency / Q000235:genetics / Q000276:immunology / Q000502:physiology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D009154:Mutation; D013270:Stomach / Q000382:microbiology
D015847:Interleukin-4; D007371:Interferon-gamma