abstract
- © 2021 Cambridge University Press. All rights reserved.T. vaginalis causes trichomoniasis, an inflammatory process related to increased rate of HIV transmission. In order to study T. vaginalis infection response in a microorganism free environment, an infection model was established providing a host-parasite interaction system useful to study the interplay between immune cells and the parasite. Infected mice peritoneal cells were immunophenotyped at different times after infection using flow cytometry. Neutrophils and macrophages showing the most relevant increase from third to twelfth day post-infection. A high number of B lymphocytes were present at fifteenth day post-infection, and an increase in memory T cells was observed at sixth day post-infection. Levels of NO increased at day 10 post-infection, no significant influence was observed on T. vaginalis clearance. Increased viability of T. vaginalis was observed when the NETs inhibitors, metformin and Cl- amidine, were administrated, highlining the importance of this mechanism to control parasite infection (43% and 86%, respectively). This report presents a comprehensive cell count of the immune cells participating against trichomoniasis in an in vivo interaction system. These data highlight the relevance of innate mechanisms such as specific population changes of innate immune cells and its impact on the T. vaginalis viability.