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Infection and Immunity, August 2001, p. 4808-4815, Vol. 69, No. 8
Departamento de Patología Animal
(Sanidad Animal)1 and Departamento de
Histologia y Anatomía Patológica,2
Facultad de Veterinaria, Universidad de Murcia, Campus de Espinardo,
30100 Murcia, Spain
Received 26 February 2001/Returned for modification 17 March
2001/Accepted 14 May 2001
A Th1 immune response involving gamma interferon (IFN-
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.8.4808-4815.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Endogenous Interleukin-12 Is Not Required for
Resolution of Chlamydophila abortus (Chlamydia
psittaci Serotype 1) Infection in Mice
)
production is required to eliminate Chlamydophila abortus
infections. In this study, the role of interleukin-12 (IL-12) in
protecting against C. abortus infection was investigated
using IL-12
/
and wild-type (WT) C57BL/6 mice to
determine the role of this Th1-promoting cytokine.
IL-12
/
mice were able to eliminate the C. abortus infection in a primary infection. However, there was a
delay in the clearance of bacteria when IL-12
/
mice
were infected with a sublethal dose of C. abortus, the
delay being associated with a lower production of IFN-
. The low
level of IFN-
was essential for survival of IL-12
/
infected mice. Both WT and IL-12
/
mice developed a Th1
immune response against C. abortus infection, since they
both produced IFN-
and immunoglobulin G2a antibody isotype. In
addition, when mice were given a secondary infectious challenge with
C. abortus, a protective host response which resolved the
secondary infection was developed by both WT and IL-12
/
mice. The lack of IL-12 resulted in few infiltrating CD4+ T
cells in the liver relative to the number in WT mice, although the
number of CD8+ T cells was slightly higher. The more
intense Th1 response presented by WT mice may have a pathogenic effect,
as the animals showed higher morbidity after the infection. In
conclusion, these results suggest that although IL-12 expedites the
clearance of C. abortus infection, this cytokine is not
essential for the establishment of a protective host response against
the infection.
*
Corresponding author. Mailing address: Departamento de
Patología Animal (Sanidad Animal), Facultad de Veterinaria,
Universidad de Murcia, Campus de Espinardo, 30100 Murcia, Spain. Phone:
34 968 364729. Fax: 34 968 364147. E-mail:
jsalinas{at}fcu.um.es.
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