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-Dependent, IFN-
Secretion by Bone Marrow-Derived Macrophages Controls an Intracellular Bacterial Infection
,
,
*
Microbiology and Tumorbiology Center,
Department of Microbiology, Pathology, and Immunology, Division of Biomedical Laboratory Technology, and Departments of
Rheumatology, Center of Molecular Medicine, and
Rheumatology, Astrid Lindgren’s Hospital, Karolinska Institutet, Stockholm, Sweden
Several reports have indicated that cell lineages apart from NK and
T cells can also express IFN-
. However, the biological relevance of
this finding is uncertain. We show in this study that bone
marrow-derived macrophages (BMMs) express IFN- at the mRNA and
protein level early after infection with Chlamydia
pneumoniae. Increased IFN- mRNA accumulation by
infected BMMs is early, transient, and requires both bacterial and host
protein synthesis. The induction of IFN- mRNA levels is independent
of IL-12 and was dramatically enhanced in IL-10-/- BMMs.
Such IL-10-/- BMMs contained less bacteria than the
wild-type controls, whereas IFN-R-/- BMMs showed
increased C. pneumoniae load. Inducible NO synthase
(iNOS) also participates in the control of bacterial load, as shown by
the enhanced numbers of C. pneumoniae in
iNOS-/- BMMs. However, the increased accumulation of iNOS
mRNA and NO in C. pneumoniae-infected BMMs depended on
the presence of IFN-
, but was independent of IFN-.
Interestingly, IFN- are also required for increased IFN- mRNA
accumulation in C. pneumoniae-infected BMMs.
Accordingly, IFN-R-/- BMMs showed higher levels of
C. pneumoniae than wild-type BMMs. Our findings unravel
an autocrine/paracrine macrophage activation pathway by showing an
IFN--dependent IFN- and iNOS induction in response to
infection, which protects macrophages against intracellular bacterial
growth.
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