TvLG is a lipid-anchored glycoconjugate that contains N-acetyllactosamine repeats that are important for attachment to vaginal epithelial cells [52]. TvLG has been associated with induction of IL-8 and MIP-3α from vaginal, ectocervical and endocervical epithelial cells. Signaling can occur through NF-κB and ERK-1 and ERK-2. Tritrichomonas foetus LPG had no effect [53] and [54]. Human galectin-1 is the first human host-receptor identified in the pathogenesis of Tv and is a receptor for TvLG [55]. Tv has many mechanisms for combating host cell defenses.

Secreted antibodies are degraded by Tv cysteine proteases such as TvCP39 [56]. Proteases also function to obviate complement lysis. An iron-rich environment induces Tv resistance to complement mediated lysis by the alternative pathway [57]. CP are thought selleckchem to target and degrade C3 of the complement pathway, but have yet to be identified [57]. Adhesin proteins play a special role as homologues of host metabolic enzymes, an example of molecular mimicry [50]. Lastly, Tv is capable of inducing apoptosis in cells of the innate immune system, notably neutrophils and macrophages, resulting

in lymphocyte tolerance (anergy). Other immune evasion mechanisms are also thought to be present [50]. As previously stated, Tv is a highly prevalent, underdiagnosed, often asymptomatic, highly communicable infection with underappreciated Bcl-2 inhibitor implications of birth related prematurity, fetal loss and increased HIV transmission and acquisition. Without universally applied, highly sensitive diagnostic methods, population screening, and mandating Tv as a reportable disease, the true burden will remain unknown and underestimated. Hoots and colleagues [58] discuss the guidelines for implicating a disease as reportable. The seven criteria were

frequency, severity, disparities or inequities associated with the health-related event, costs associated with the health-related event, Dipeptidyl peptidase preventability, communicability, and public interest. The assessment concluded that frequency, disparities or inequities, and communicability of Tv are fulfilled [58]. Unfortunately public interest is sadly lacking. Therefore in the absence of being a reportable disease we propose that a vaccine would be a cheap, easily administered prophylactic means to prevent and reduce incidence and prevalence of Tv globally, even in low income settings. Our lab has previously reported the use of a mouse model for experimental vaginal Tv infection and inducible immunity [59]. Within this model, mice are treated with estradiol to synchronize mice into estrus, a factor associated with initial infectivity of Tv. Additionally, Lactobacillus acidophilus, found in normal human vaginal flora of the majority of women [60], is inoculated into the vagina of mice resulting in a vaginal pH resembling the human vagina, and contributes to chronicity of infection in mice [61] and [62].