The complex fibronectin--Trichomonas vaginalis interactions and Trichomonosis.

摘要: Abstract Trichomonosis is the vaginitis caused by Trichomonas vaginalis . This sexually transmitted agent achieves successful host parasitism through various means including: (1) acquisition of nutrients specific receptors; (2) recognition and binding to mucin followed cytoadherence mediated adhesins that resemble metabolic enzymes; (3) evasion immune responses (i) masking organisms proteins, (ii) shedding trichomonad proteins into secretions (iii) cysteine proteinases degrade all immunoglobulin subclasses complement; (4) alternating surface expression at least two antigen repertoires; (5) alternate coordinate virulence genes in response environmental factors. The fact parasite survives long term varying adverse environment vagina attests highly evolved nature this protist. An understanding non-self-limiting infection may come from recent findings illustrating complexity –fibronectin (FN) interactions. readily attaches surfaces with immobilized FN binds a receptor-mediated fashion. amount affinity bound live influenced concentrations medium both iron calcium. De novo protein synthesis required for optimal presence Furthermore, parasites bind differing affinities N-terminal domain (NTD), cell-binding (CBD) gelatin-binding (GBD) FN. Iron modulates NTD similar minireview summarizes on T. –FN associations.