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Iron mediates Trichomonas vaginalis resistance to complement lysis
J F Alderete1, D Provenzano, M W Lehker
1Department of Microbiology, University of Texas Health Science Center, San Antonio 78284-7758, USA.
Microbial Pathogenesis
|August 1, 1995
Summary
Trichomonas vaginalis parasites become resistant to complement lysis when grown with iron. This iron-induced resistance is mediated by a proteinase that degrades complement component C3.
Area of Science:
- Parasitology
- Immunology
- Molecular Biology
Background:
- Trichomonas vaginalis is a human sexually transmitted pathogen.
- The alternative complement pathway is crucial for innate immunity against T. vaginalis.
- Iron availability is a key factor in host-pathogen interactions.
Purpose of the Study:
- To investigate the role of iron in T. vaginalis resistance to complement-mediated lysis.
- To elucidate the mechanism by which iron confers resistance.
- To identify potential therapeutic targets for enhancing complement-mediated killing.
Main Methods:
- Culturing T. vaginalis in iron-depleted and iron-supplemented media.
- Assessing parasite survival after complement activation.
- Evaluating the effect of iron concentration and other divalent cations on resistance.
- Testing the ability of lactoferrin and transferrin to modulate resistance.
- Investigating the role of proteinases using proteinase inhibitors.
Main Results:
- Parasites grown in iron-supplemented medium were resistant to complement lysis, while those in iron-depleted medium were susceptible.
- Complement resistance was directly dependent on iron concentration.
- Lactoferrin, but not transferrin, conferred resistance to low-iron parasites.
- Proteinase inhibitors restored complement susceptibility to high-iron parasites.
- Resistance is likely due to proteinase-mediated degradation of C3 on the parasite surface.
Conclusions:
- Iron acquisition is a critical factor for T. vaginalis immune evasion.
- Iron-dependent proteinase activity degrades complement component C3, conferring resistance.
- Targeting this iron-regulated proteinase may represent a novel therapeutic strategy against trichomoniasis.