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Review
. 2020 Sep;10(9):200192.
doi: 10.1098/rsob.200192. Epub 2020 Sep 2.

Neutrophil interactions with the sexually transmitted parasite Trichomonas vaginalis: implications for immunity and pathogenesis

Affiliations
Review

Neutrophil interactions with the sexually transmitted parasite Trichomonas vaginalis: implications for immunity and pathogenesis

Suhani B Bhakta et al. Open Biol. 2020 Sep.

Abstract

Trichomoniasis is the third most common sexually transmitted infection in humans and is caused by the protozoan parasite, Trichomonas vaginalis (Tv). Pathogenic outcomes are more common in women and generally include mild vaginitis or cervicitis. However, more serious effects associated with trichomoniasis include adverse reproductive outcomes. Like other infectious agents, pathogenesis from Tv infection is predicted to be the result of both parasite and host factors. At the site of infection, neutrophils are the most abundant immune cells present and probably play key roles in both parasite clearance and inflammatory pathology. Here, we discuss the evidence that neutrophils home to the site of Tv infection, kill the parasite, and that in some circumstances, parasites possibly evade neutrophil-directed killing. In vitro, the parasite is killed by neutrophils using a novel antimicrobial mechanism called trogocytosis, which probably involves both innate and adaptive immunity. While mechanisms of evasion are mostly conjecture at present, the persistence of Tv infections in patients argues strongly for their existence. Additionally, many strains of Tv harbour microbial symbionts Mycoplasma hominis or Trichomonasvirus, which are both predicted to impact neutrophil responses against the parasite. Novel research tools, especially animal models, will help to reveal the true outcomes of many factors involved in neutrophil-Tv interactions during trichomoniasis.

Keywords: Mycoplasma hominis; Trichomonas vaginalis; inflammation; neutrophil; sexually transmitted infection; trogocytosis.

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Conflict of interest statement

We declare we have no competing interests.

Figures

Figure 1.
Figure 1.
Neutrophils flow rapidly through blood, but activation of the endothelium by inflammatory mediators near an infection site can begin the process of neutrophil extravasation through diapedesis. Inflammatory mediators are secreted in response to Tv (green) from epithelial cells (pink), resident macrophages (purple) and neutrophils that arrive first (pink cells with multi-lobed nuclei). The greatest amount of inflammatory cytokines is triggered by strains of Tv that harbour symbionts Mycoplasma hominis or Trichomonasvirus. Once out of the blood, neutrophils follow IL-8 and LTB4 gradients to home to parasites. Upon encountering Tv, neutrophils swarm and trogocytose the parasite.

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