Trichomoniasis immunity and the involvement of the purinergic signaling

Abstract

Innate and adaptive immunity play a significant role in trichomoniasis, the most common non-viral sexually transmitted disease worldwide. In the urogenital tract, innate immunity is accomplished by a defense physical barrier constituted by epithelial cells, mucus, and acidic pH. During infection, immune cells, antimicrobial peptides, cytokines, chemokines, and adaptive immunity evolve in the reproductive tract, and a proinflammatory response is generated to eliminate the invading extracellular pathogen Trichomonas vaginalis. However, the parasite has developed complex evolutionary mechanisms to evade the host immune response through cysteine proteases, phenotypic variation, and molecular mimicry. The purinergic system constitutes a signaling cellular net where nucleotides and nucleosides, enzymes, purinoceptors and transporters are involved in almost all cells and tissues signaling pathways, especially in central and autonomic nervous systems, endocrine, respiratory, cardiac, reproductive, and immune systems, during physiological as well as pathological processes. The involvement of the purinergic system in T. vaginalis biology and infection has been demonstrated and this review highlights the participation of this signaling pathway in the parasite immune evasion strategies.

Humoral and T cell–mediated immune response against trichomoniasis

“…The presence of T. vaginalis ‐specific IgG, IgM, IgA and IgG antibodies has been demonstrated by different techniques. In addition, the presence of IgE was also found in genital specimens from infected individuals at low concentrations . The seroprevalence and the levels of T. vaginalis‐ specific IgG, IgA and IgM were higher in serum and vaginal secretions from T. vaginalis‐ infected subjects compared to the uninfected individuals …”

“…The innate, local, nonspecific defense mechanisms against T. vaginalis include activation of alternative pathway of the complement system, induction of toll‐like receptors (TLRs) and abundant accumulation of polymorphonuclear neutrophils and macrophages . The pathogen is susceptible to direct complement‐mediated killing, and complement activation provides C3 opsonin that promotes neutrophil‐mediated phagocytosis of T. vaginalis but high iron‐induced cysteine proteases protect the parasite from complement‐related lysis .…”

“…It has been indicated that the T. vaginalis ‐specific IgG enhances LTB4 production by neutrophils via a complement activation‐related process. Nevertheless, a number of studies reported that the antibody‐mediated immunity is transient, and there is little evidence on its efficacy in parasite elimination . The lack of effective and persistent humoral immunity is one of the challenges in designing a protective vaccine for trichomoniasis …”

“…Levels of TvLPG‐specific IgA in vaginal secretions from women with trichomoniasis were also higher than control subjects. In addition, the T. vaginalis ‐infected women with normal pregnancies had higher levels of TvLPG‐specific IgG in their vaginal secretions than infected women with adverse outcomes in their pregnancies . It is suggested that the vaginal TvLPG‐specific IgG may be protective against adverse outcome of pregnancies and may even decrease the risk for HIV transmission.…”

“…Both innate and adaptive immune responses are activated during T. vaginalis infection . Some studies suggested that the humoral immunity is transient and not persistent, and there is little evidence on its efficacy in the in vivo elimination of parasite . Innate immunity plays a prominent role in the protection and elimination of parasite during trichomoniasis .…”