Authors

Discussion

Species members of the Trichomonas genus are responsible for disease in several animal species including Humans. Most notably Trichomonas vaginalis, the most common non-viral STI for humans, causes trichomoniasis, which is strongly associated with increased susceptibility to other important pathogens such as HIV and HPV.

Trichomonas species live at various mucosal surfaces characterised by complex microbiota amongst a wide range of animal hosts. Trichomonas infections are associated with significant changes in the microbiota’s taxonomic composition commonly referred to as dysbiosis when associated with diseases. Notably, infections with Trichomonas vaginalis and Trichomonas gallinae (a bird parasite) result in the depletion of the mutualist bacteria Lactobacillus spp., known to play numerous important roles in female urogenital defence against pathogens. However, the molecular and cellular basis of interactions between Trichomonas and members of the microbiota are poorly understood.

We exploited Trichomonas gallinae in co-culture with Escherichia coli as a model system in combination with comparative genomics and transcriptomics (RNAseq) to identify candidate enzymes and peptides targeting bacteria. A number of genes encoding homologues of bacterial cell wall targeting enzymes, including candidate lysozymes, and anti-microbial peptides, both of which are conserved throughout Trichomonas spp., were identified and with a number of them shown to be significantly upregulated within the co-culture system. We also observed changes in bacterial and parasite behaviour and morphology.

Integrating comparative genomics between species, transcriptomics within our model and already known interactions between Trichomonas and bacteria; involving for example the peptidoglycan targeting NlpC/P60 endopeptidases; illustrates a number of mechanisms for the parasites to potentially out-compete neighbouring bacteria, with a likely important role of deconstructing bacterial cell wall peptidoglycans. This could be to extract nutrients from the microbiota and/or alter the microbiota to produce a more hospitable host environment for the Trichomonas. This could lead to the promotion of Trichomonas species growth within an infected individual and through dysbiosis, could also contribute at promoting damaging host tissue inflammations. Furthermore, the conserved ability to target the bacteria from the microbiota could contribute to enabling zoonosis.

Together these findings bring new insights into the molecular and cellular basis of Trichomonas-Bacterial interactions and how these evolutionary conserved interactions, gained through several lateral gene transfers from bacteria, can potentially influence the zoonotic ability of Trichomonas.