title: Endogenous interleukin-12 is not required for resolution of Chlamydophila abortus (Chlamydia psittaci serotype 1) infection in mice.
abstract: A Th1 immune response involving gamma interferon (IFN-gamma) 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-gamma. The low level of IFN-gamma 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-gamma 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.
authors.affiliation: Departamento de Patología Animal (Sanidad Animal), Facultad de Veterinaria, Universidad de Murcia, Campus de Espinardo, 30100 Murcia, Spain.
authors.forename: L
authors.initials: L
authors.lastname: Del Río
authors.forename: A J
authors.initials: AJ
authors.lastname: Buendía
authors.forename: J
authors.initials: J
authors.lastname: Sánchez
authors.forename: M C
authors.initials: MC
authors.lastname: Gallego
authors.forename: M R
authors.initials: MR
authors.lastname: Caro
authors.forename: N
authors.initials: N
authors.lastname: Ortega
authors.forename: J
authors.initials: J
authors.lastname: Seva
authors.forename: F J
authors.initials: FJ
authors.lastname: Pallarés
authors.forename: F
authors.initials: F
authors.lastname: Cuello
authors.forename: J
authors.initials: J
authors.lastname: Salinas
mesh_terms: D000818:Animals; D018791:CD4 Lymphocyte Count; D015496:CD4-Positive T-Lymphocytes / Q000166:cytology; D002691:Chlamydophila psittaci / Q000276:immunology; D004195:Disease Models, Animal; D005260:Female; D007371:Interferon-gamma / Q000096:biosynthesis / Q000276:immunology; D018664:Interleukin-12 / Q000276:immunology*; D020382:Interleukin-18 / Q000096:biosynthesis; D008099:Liver / Q000166:cytology / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009017:Morbidity; D009956:Psittacosis / Q000453:epidemiology / Q000276:immunology* / Q000473:pathology; D018418:Th2 Cells / Q000276:immunology
chemical_list: D020382:Interleukin-18; D018664:Interleukin-12; D007371:Interferon-gamma