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*
Institut für Medizinische Mikrobiologie und Hygiene, Universitätsklinikum Mannheim, Universität Heidelberg, Germany;
Institut für Neuropathologie, Universitätskliniken Bonn, Bonn, Germany; and
Institut für Klinische Mikrobiologie, Immunologie und Hygiene, Universität Erlangen, Erlangen, Germany
Infection of C57BL/6 mice with Toxoplasma gondii
leads to progressive and ultimately fatal chronic
Toxoplasma encephalitis (TE). Genetic deletion or
inhibition of inducible nitric oxide synthase (iNOS) from the beginning
of infection increased the number of T. gondii cysts in
the brain and markedly reduced the time-to-death in this mouse strain.
In the present study, we addressed whether iNOS also contributes to the
control of intracerebral parasites in a clinically stable latent
infection that develops in T. gondii-resistant BALB/c
mice after resolution of the acute phase of TE. iNOS was expressed in
the inflammatory cerebral infiltrates of latently infected BALB/c mice,
but the number of iNOS+ cells was significantly lower than
in the brains of chronically infected T.
gondii-susceptible C57BL/6 mice. In BALB/c mice with latent TE
(>30 days of infection), treatment with the iNOS inhibitors
L-N6-iminoethyl-lysine or
L-nitroarginine-methylester for 
40 days did not result in
an increase of the intracerebral parasitic load and a reactivation of
the disease, despite the presence of iNOS-suppressive inhibitor levels
in the brain. However, L-nitroarginine-methylester
treatment had remarkably toxic effects and induced a severe wasting
syndrome with high mortality. In contrast to BALB/c mice,
L-N6-iminoethyl-lysine treatment
rapidly exacerbated the already established chronic TE of C57BL/6 mice.
Thus, the containment of latent toxoplasms in T.
gondii-resistant BALB/c mice is independent of iNOS, whereas
the temporary control of intracerebral parasites in T.
gondii-susceptible C57BL/6 mice with chronic TE requires iNOS
activity.
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