title: Sequestration of host-CD59 as potential immune evasion strategy of Trichomonas vaginalis.
abstract: Trichomonas vaginalis is known to evade complement-mediated lysis. Because the genome of T. vaginalis does not possess DNA sequence with homology to human protectin (CD59), a complement lysis restricting factor, we tested the hypothesis that host CD59 acquisition by T. vaginalis organisms mediates resistance to complement killing. This hypothesis was based on the fact that trichomonads are known to associate with host proteins. No CD59 was detected on the surface of T. vaginalis grown in serum-based medium using as probe anti-CD59 monoclonal antibody (MAb). We, therefore, infected mice intraperitoneally with live T. vaginalis, and trichomonads harvested from ascites were tested for binding of CD59. Immunofluorescence showed that parasites had surface CD59. Furthermore, as mouse erythrocytes (RBCs) possess membrane-associated CD59, and trichomonads use RBCs as a nutrient source, organisms were co-cultured with murine RBCs for one week. Parasites were shown to have detectable surface CD59. Importantly, live T. vaginalis with bound CD59 were compared with batch-grown parasites without surface-associated CD59 for sensitivity to complement in human serum. Trichomonads without surface-bound CD59 had a higher level of killing by complement than did parasites with surface CD59. These data show that host CD59 acquired onto the surface by live T. vaginalis may be an alternative mechanism for complement evasion. We describe a novel strategy by T. vaginalis consistent with host protein procurement by this parasite to evade the lytic action of complement.
authors.affiliation: CEI Campus Moncloa, UCM-UPM and CSIC, Madrid, Spain; Department of Parasitology, Faculty of Pharmacy, Universidad Complutense de Madrid, Spain. Electronic address: alexandraibanez@ucm.es.
authors.forename: Alexandra
authors.initials: A
authors.lastname: Ibáñez-Escribano
authors.affiliation: CEI Campus Moncloa, UCM-UPM and CSIC, Madrid, Spain; Department of Parasitology, Faculty of Pharmacy, Universidad Complutense de Madrid, Spain.
authors.forename: Juan José
authors.initials: JJ
authors.lastname: Nogal-Ruiz
authors.affiliation: Department of Biomedicine and Biotechnology, School of Pharmacy, University of Alcalá de Henares, Madrid, Spain.
authors.forename: Jorge
authors.initials: J
authors.lastname: Pérez-Serrano
authors.affiliation: CEI Campus Moncloa, UCM-UPM and CSIC, Madrid, Spain; Department of Parasitology, Faculty of Pharmacy, Universidad Complutense de Madrid, Spain.
authors.forename: Alicia
authors.initials: A
authors.lastname: Gómez-Barrio
authors.affiliation: CEI Campus Moncloa, UCM-UPM and CSIC, Madrid, Spain; Department of Parasitology, Faculty of Pharmacy, Universidad Complutense de Madrid, Spain.
authors.forename: J Antonio
authors.initials: JA
authors.lastname: Escario
authors.affiliation: School of Molecular Bioscience, College of Veterinary Medicine, Washington State University, Pullman, WA, USA.
authors.forename: J F
authors.initials: JF
authors.lastname: Alderete
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal; D018957:CD59 Antigens / Q000378:metabolism*; D003165:Complement System Proteins / Q000276:immunology*; D004912:Erythrocytes / Q000276:immunology*; D005455:Fluorescent Antibody Technique; D006801:Humans; D057131:Immune Evasion; D051379:Mice; D014246:Trichomonas vaginalis / Q000235:genetics / Q000378:metabolism / Q000472:pathogenicity*
chemical_list: D000911:Antibodies, Monoclonal; D018957:CD59 Antigens; D003165:Complement System Proteins
keywords: Ascites; CD59; Complement; Erythrocytes; Fluorescence; Human sera; Immune evasion; Trichomonas vaginalis