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in the Mouse Placenta During Listeria monocytogenes Infection1
* Center for the Study of Reproductive Biology and Women’s Health, Department of Developmental and Molecular Biology and
Obstetrics and Gynecology and Women’s Health, Albert Einstein College of Medicine, Bronx, NY 10461; and
Department of Pharmacology, Hokkaido University School of Medicine, Sapporo, Japan
The tryptophan-catabolizing enzyme indoleamine 2,3-dioxygenase
(IDO) is expressed in macrophages that have been differentiated in the
presence of CSF-1 and is important in the containment of intracellular
pathogens. IDO also appears to play a role in suppression of T cell
responses in a variety of contexts. In the placenta, its enzymatic
activity is believed to establish a chemical barrier that protects the
fetal allograft from T cell-mediated immune aggression. We have studied
the regulation of IDO in the utero-placental unit of mice following
infection with the Gram-positive, intracellular bacterium
Listeria monocytogenes that has a predilection for
replication in the decidua basalis. IDO mRNA and protein expression is
enhanced in the utero-placental unit following infection with L.
monocytogenes. However, in contrast to the human where IDO is
expressed by the CSF-1R-positive syncytial trophoblast, IDO is not
expressed in murine trophoblastic tissue but instead is found in
stromal cells of the decidua basalis and metrial gland and following
infection, in endothelial cells. Using mice carrying null mutations in
cytokine/growth factor genes, we explored the regulation of IDO in the
placenta. Consistent with the absence of CSF-1R expression in the
IDO-expressing cells of mice, neither the basal levels of IDO nor its
induction following infection is affected by the absence of CSF-1.
However, although the basal level of IDO is normal, the enhanced
expression during Listeriosis is completely abrogated in the absence of
IFN-
, a cytokine required for the resolution of this infection.
These data suggest that IDO plays a role in resolving bacterial
infection in the placenta while at the same time maintaining a barrier
to T cells whose presence might result in fetal
rejection.
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