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Infection and Immunity, April 2000, p. 2245-2253, Vol. 68, No. 4
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Roles of Interleukin-12 and Gamma Interferon in Murine Chlamydia pneumoniae Infection

Yuemei Geng,1,dagger Klara Berencsi,1 Zsofia Gyulai,1 Tibor Valyi-Nagy,2 Eva Gonczol,1 and Giorgio Trinchieri1,*

The Wistar Institute of Anatomy and Biology, Philadelphia, Pennsylvania 19104,1 and Vanderbilt University Medical Center, Nashville, Tennessee 372322

Received 22 July 1999/Returned for modification 21 October 1999/Accepted 2 December 1999

BALB/c and strain 129 mice infected intranasally with Chlamydia pneumoniae displayed a moderate-to-severe inflammation in the lungs and produced interleukin-12 (IL-12), gamma interferon (IFN-gamma ), tumor necrosis factor alpha (TNF-alpha ), and IL-10, with peak levels on days 1 to 3 postinfection (p.i.), returning to basal levels by day 16 p.i. Anti-IL-12 treatment resulted in less-severe pathological changes but higher bacterial titers on days 3 and 7 p.i. By day 16 p.i., the inflammatory responses of control antibody-treated mice subsided. The bacterial titers of both anti-IL-12- and control antibody-treated mice decreased within 3 weeks to marginally detectable levels. Anti-IL-12 treatment significantly reduced lung IFN-gamma production and in vitro spleen cell IFN-gamma production in response to either C. pneumoniae or concanavalin A. In gamma -irradiated infected mice, cytokine production was delayed, and this delay correlated with high bacterial titers in the lungs. Following C. pneumoniae infection, 129 mice lacking the IFN-gamma receptor alpha  chain gene (G129 mice) produced similar IL-12 levels and exhibited similarly severe pathological changes but had higher bacterial titers than 129 mice. However, by day 45 p.i., bacterial titers became undetectable in both wild-type 129 and G129 mice. Thus, during C. pneumoniae lung infection, IL-12, more than IFN-gamma , plays a role in pulmonary-cell infiltration. IFN-gamma and IL-12, acting mostly through its induction of IFN-gamma and Th1 responses, play an important role in controlling acute C. pneumoniae infection in the lungs, but eventually all mice control the infection to undetectable levels by IL-12- and IFN-gamma -independent mechanisms.

* Corresponding author. Present address: Schering-Plough Laboratory of Immunological Research, 27 Chemin des Peupliers, BP 11, 69571 Dardilly Cedex, France. Phone: 33 472 17 2740. Fax: 33 478 35 4750. E-mail: giorgio.trinchieri{at}spcorp.com.

dagger Present address: Department of Dermatology, University of Pennsylvania, Philadelphia, PA 19104.

Infection and Immunity, April 2000, p. 2245-2253, Vol. 68, No. 4
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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