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Infection and Immunity, April 2000, p. 2245-2253, Vol. 68, No. 4
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-
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

), tumor necrosis factor alpha (TNF-
), 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-
production and in vitro spleen cell IFN-
production in response to either C. pneumoniae or
concanavalin A. In
-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-
receptor
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-
, plays a role in pulmonary-cell infiltration. IFN-
and IL-12, acting mostly through its induction of
IFN-
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-
-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.
Present address: Department of Dermatology, University of
Pennsylvania, Philadelphia, PA 19104.
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