Linked Life Data

10092808

Source:http://linkedlifedata.com/resource/pubmed/id/10092808

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1999-4-13
pubmed:abstractText
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 < or = 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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
162
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3512-8
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:10092808-Administration, Oral, pubmed-meshheading:10092808-Animals, pubmed-meshheading:10092808-Brain, pubmed-meshheading:10092808-Chronic Disease, pubmed-meshheading:10092808-Encephalitis, pubmed-meshheading:10092808-Enzyme Induction, pubmed-meshheading:10092808-Enzyme Inhibitors, pubmed-meshheading:10092808-Female, pubmed-meshheading:10092808-Genetic Predisposition to Disease, pubmed-meshheading:10092808-Immunity, Innate, pubmed-meshheading:10092808-Kinetics, pubmed-meshheading:10092808-Lysine, pubmed-meshheading:10092808-Mice, pubmed-meshheading:10092808-Mice, Inbred BALB C, pubmed-meshheading:10092808-Mice, Inbred C57BL, pubmed-meshheading:10092808-NG-Nitroarginine Methyl Ester, pubmed-meshheading:10092808-Nitric Oxide Synthase, pubmed-meshheading:10092808-Nitric Oxide Synthase Type II, pubmed-meshheading:10092808-Species Specificity, pubmed-meshheading:10092808-Toxoplasma, pubmed-meshheading:10092808-Toxoplasmosis, Animal, pubmed-meshheading:10092808-Toxoplasmosis, Cerebral
pubmed:year
1999
pubmed:articleTitle
Inhibition of inducible nitric oxide synthase exacerbates chronic cerebral toxoplasmosis in Toxoplasma gondii-susceptible C57BL/6 mice but does not reactivate the latent disease in T. gondii-resistant BALB/c mice.
pubmed:affiliation
Institut für Medizinische Mikrobiologie und Hygiene, Universitätsklinikum Mannheim, Universität Heidelberg, Germany.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't