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Infect Immun, July 1998, p. 3142-3148, Vol. 66, No. 7
Division of Comparative Medicine,
Massachusetts Institute of Technology, Cambridge, Massachusetts
02139
Received 19 December 1997/Returned for modification 4 March
1998/Accepted 23 April 1998
Helicobacter hepaticus infection in A/JCr
mice results in chronic active hepatitis characterized by perivascular,
periportal, and parenchymal infiltrates of mononuclear and
polymorphonuclear cells. This study examined the development of
hepatitis and the immune response of A/JCr mice to H. hepaticus infection. The humoral and cell-mediated T
helper immune response was profiled by measuring the postinfection
(p.i.) antibody response in serum, feces, and bile and by the
production of cytokines and proliferative responses by splenic
mononuclear cells to H. hepaticus
antigens. Secretory immunoglobulin A (IgA) and systemic IgG2a
antibody developed by 4 weeks p.i. and persisted through 12 months.
Splenocytes from infected mice proliferated and produced more gamma
interferon (IFN-
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Chronic Active Hepatitis Induced by Helicobacter
hepaticus in the A/JCr Mouse Is Associated with a
Th1 Cell-Mediated Immune Response
) than interleukin-4 (IL-4) or IL-5 when cultured
with H. hepaticus outer membrane proteins. The
predominantly IgG2a antibody response in serum and the in vitro
production of IFN-
in excess of IL-4 or IL-5 are consistent with a
Th1 immune response reported in humans and mice infected with
Helicobacter pylori and Helicobacter felis,
respectively. Mice infected with H. hepaticus developed progressively severe
perivascular, periportal, and hepatic parenchymal lesions consisting of
lymphohistiocytic and plasmacytic cellular infiltrates. In addition,
transmural typhlitis was observed at 12 months p.i. The
characterization of a cell-mediated Th1 immune response to
H. hepaticus infection in the A/JCr mouse
should prove valuable as a model for experimental regimens which
manipulate the host response to Helicobacter.
*
Corresponding author. Mailing address: Division of
Comparative Medicine, Massachusetts Institute of Technology, 77 Massachusetts Ave., Bldg. 16-825A, Cambridge, MA 02139. Phone: (617)
253-1757. Fax: (617) 258-5708. E-mail: mwhary{at}mit.edu.
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