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Infection and Immunity, June 2002, p. 3295-3299, Vol. 70, No. 6
0019-9567/02/$04.00+0 DOI: 10.1128/IAI.70.6.3295-3299.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
Role of Gamma Interferon in Helicobacter pylori Induction of Inflammatory Mediators during Murine Infection
Marygorret Obonyo,1 Donald G. Guiney,1 Julia Harwood,1 Joshua Fierer,1,2,3 and Sheri P. Cole1*
Department of Medicine,1
Department of Pathology, School of Medicine, University of California, San Diego, La Jolla, California 92093,2
VA San Diego Healthcare System, San Diego, California 921613
Received 17 September 2001/
Returned for modification 9 November 2001/
Accepted 14 March 2002
Gamma interferon (IFN-
) has been proposed to play an important role in Helicobacter-related gastritis. Using the IFN-
gene knockout (IFN-
-/-) mouse model and a murine gastric epithelial cell line, GSM06, we demonstrated that Helicobacter pylori maximally induced macrophage inflammatory protein-2 (MIP-2) and inducible nitric oxide synthase (iNOS) mRNA only in wild-type mice. MIP-2 and iNOS mRNA were also induced by H. pylori in GSM06 cells. Induction of cyclooxygenase 2 mRNA through IFN-
was demonstrated in GSM06 cells. These data indicate that IFN-
mediates the induction of MIP-2 and iNOS mRNA expression by H. pylori in mice.
* Corresponding author. Mailing address: Department of Medicine, School of Medicine, University of California, San Diego, 9500 Gilman Dr., La Jolla, CA 92023-0640. Phone: (858) 534-6024. Fax: (858) 534-6020. E-mail:
scole{at}ucsd.edu.
Editor: R. N. Moore
Infection and Immunity, June 2002, p. 3295-3299, Vol. 70, No. 6
0019-9567/02/$04.00+0 DOI: 10.1128/IAI.70.6.3295-3299.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
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