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Infection and Immunity, September 2000, p. 5107-5113, Vol. 68, No. 9
Center for Gastrointestinal Biology and
Disease, University of North Carolina at Chapel
Hill,1 and Department of Microbiology,
University of North Carolina Hospitals,3 Chapel
Hill, and College of Veterinary Medicine, North Carolina
State University, Raleigh,2 North
Carolina, and Departments of Surgery and Microbiology,
University of Wisconsin, Madison, Wisconsin4
Received 15 October 1999/Returned for modification 22 December
1999/Accepted 6 June 2000
Helicobacter hepaticus has been reported to induce
colitis, hepatitis, and hepatocellular carcinoma in several different
murine models. The aim of this study was to determine if H. hepaticus will cause colitis in monoassociated mice lacking the
interleukin-10 gene (IL-10
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Helicobacter hepaticus Does Not Induce
or Potentiate Colitis in Interleukin-10-Deficient Mice
/
mice) and potentiate
colitis in specific-pathogen-free (SPF) IL-10
/
mice.
Germfree IL-10
/
mice on either a mixed (C57BL/6 × 129/Ola) or inbred (129/SvEv) genetic background were monoassociated
with H. hepaticus ATCC 51448 by oral feeding and rectal
enemas. In a second experiment, germfree IL-10
/
mice
were colonized with stool from SPF mice that harbored or did not harbor
endogenous H. hepaticus. After 7 to 9 weeks of colonization, weight loss and mortality were assessed, the colon was
isolated for histology and IL-12 secretion, and mesenteric lymph node
cells were assessed for T-cell activation markers. It was found that
IL-10
/
mice monoassociated with H. hepaticus for up to 16 weeks showed almost no histologic colitis
or increased IL-12 production. SPF IL-10-knockout mice had no
significant difference in weight loss, mortality rate, histologic
scores, colonic IL-12 secretion, or T-cell activation with or without
H. hepaticus. We conclude that H. hepaticus
does not induce or potentiate disease in our IL-10
/
mice and therefore is not required to induce colitis in genetically susceptible hosts.
*
Corresponding author. Mailing address: Division of
Digestive Diseases, Glaxo Bldg., Room 146, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7080. Phone: (919) 966-7886. Fax:
(919) 966-6842. E-mail: ldiele{at}med.unc.edu.
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