Iron enhancement of experimental infection of mice by Tritrichomonas foetus
Language English Country Germany Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
10431735
DOI
10.1007/s004360050617
Knihovny.cz E-resources
- MeSH
- Injections, Intraperitoneal MeSH
- Quaternary Ammonium Compounds administration & dosage pharmacology MeSH
- Nitrilotriacetic Acid analogs & derivatives pharmacology MeSH
- Lactoferrin pharmacology MeSH
- Disease Models, Animal MeSH
- Mice, Inbred ICR MeSH
- Mice MeSH
- Protozoan Infections mortality parasitology MeSH
- Transferrin pharmacology MeSH
- Tritrichomonas foetus growth & development pathogenicity MeSH
- Virulence MeSH
- Ferric Compounds administration & dosage pharmacology MeSH
- Ferrous Compounds administration & dosage pharmacology MeSH
- Iron metabolism MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- ferric ammonium citrate MeSH Browser
- ferric nitrilotriacetate MeSH Browser
- ferrous sulfate MeSH Browser
- Quaternary Ammonium Compounds MeSH
- Nitrilotriacetic Acid MeSH
- Lactoferrin MeSH
- Transferrin MeSH
- Ferric Compounds MeSH
- Ferrous Compounds MeSH
- Iron MeSH
The ability of a microbial invader to acquire iron from its vertebrate host has been recognized as an important virulence mechanism in some pathogenic bacteria. We examined the involvement of similar mechanisms in an experimental infection of mice by a protozoan pathogen of cattle, Tritrichomonas foetus. In a series of experiments, outbred ICR mice were inoculated intraperitoneally with two strains of T. foetus, the moderately virulent KV-1 (approximately 5% mortality rate) and the highly virulent LUB-1MIP (approximately 80% mortality rate). Treatment of mice with ferric ammonium citrate (FeAC) (100 mg/kg per day intraperitoneally) increased the mortality rate caused by the KV-1 infection up to the level determined for the highly virulent strain. The treatment effect was dose dependent and required early administration of FeAC after inoculation of parasites and its continued supply for at least 3 subsequent days. Daily sampling of peritoneal exudate showed that the infection-enhancing effect of iron overload was associated with a stimulation of parasite multiplication, which in the case of KV-1 infection was strongly suppressed in untreated mice. Consistent with these findings, the strain of lower virulence (KV-1) showed considerably lower efficiency accumulating radiolabeled iron from transferrin and a low-molecular source [Fe(III)nitrilotriacetic acid] in vitro. The results indicate an involvement of iron uptake mechanisms by the parasite as a virulence factor in T. foetus infection.
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