Trypanosoma cruzi P21 recombinant protein modulates Toxoplasma gondii infection in different experimental models of the human maternal-fetal interface.

Autor:	de Souza G; Laboratory of Immunophysiology of Reproduction, Institute of Biomedical Sciences, Universidade Federal de Uberlândia, Uberlândia, MG, Brazil., Teixeira SC; Laboratory of Immunophysiology of Reproduction, Institute of Biomedical Sciences, Universidade Federal de Uberlândia, Uberlândia, MG, Brazil., Fajardo Martínez AF; Laboratory of Immunophysiology of Reproduction, Institute of Biomedical Sciences, Universidade Federal de Uberlândia, Uberlândia, MG, Brazil., Silva RJ; Laboratory of Immunophysiology of Reproduction, Institute of Biomedical Sciences, Universidade Federal de Uberlândia, Uberlândia, MG, Brazil., Luz LC; Laboratory of Immunophysiology of Reproduction, Institute of Biomedical Sciences, Universidade Federal de Uberlândia, Uberlândia, MG, Brazil., de Lima Júnior JP; Laboratory of Immunophysiology of Reproduction, Institute of Biomedical Sciences, Universidade Federal de Uberlândia, Uberlândia, MG, Brazil., Rosini AM; Laboratory of Immunophysiology of Reproduction, Institute of Biomedical Sciences, Universidade Federal de Uberlândia, Uberlândia, MG, Brazil., Dos Santos NCL; Laboratory of Immunophysiology of Reproduction, Institute of Biomedical Sciences, Universidade Federal de Uberlândia, Uberlândia, MG, Brazil., de Oliveira RM; Laboratory of Immunophysiology of Reproduction, Institute of Biomedical Sciences, Universidade Federal de Uberlândia, Uberlândia, MG, Brazil., Paschoalino M; Laboratory of Immunophysiology of Reproduction, Institute of Biomedical Sciences, Universidade Federal de Uberlândia, Uberlândia, MG, Brazil., Barbosa MC; Laboratory of Immunophysiology of Reproduction, Institute of Biomedical Sciences, Universidade Federal de Uberlândia, Uberlândia, MG, Brazil., Alves RN; Department of Agricultural and Natural Science, Universidade do Estado de Minas Gerais, Ituiutaba, MG, Brazil., Gomes AO; Institute of Natural and Biological Sciences, Universidade Federal do Triângulo Mineiro, Uberaba, MG, Brazil., da Silva CV; Laboratory of Trypanosomatids, Institute of Biomedical Sciences, Universidade Federal de Uberlândia, Uberlândia, Brazil., Ferro EAV; Laboratory of Immunophysiology of Reproduction, Institute of Biomedical Sciences, Universidade Federal de Uberlândia, Uberlândia, MG, Brazil., Barbosa BF; Laboratory of Immunophysiology of Reproduction, Institute of Biomedical Sciences, Universidade Federal de Uberlândia, Uberlândia, MG, Brazil.
Jazyk:	angličtina
Zdroj:	Frontiers in immunology [Front Immunol] 2023 Oct 16; Vol. 14, pp. 1243480. Date of Electronic Publication: 2023 Oct 16 (Print Publication: 2023).
DOI:	10.3389/fimmu.2023.1243480
Abstrakt:	Introduction: Toxoplasma gondii is the etiologic agent of toxoplasmosis, a disease that affects about one-third of the human population. Most infected individuals are asymptomatic, but severe cases can occur such as in congenital transmission, which can be aggravated in individuals infected with other pathogens, such as HIV-positive pregnant women. However, it is unknown whether infection by other pathogens, such as Trypanosoma cruzi , the etiologic agent of Chagas disease, as well as one of its proteins, P21, could aggravate T. gondii infection. Methods: In this sense, we aimed to investigate the impact of T. cruzi and recombinant P21 (rP21) on T. gondii infection in BeWo cells and human placental explants. Results: Our results showed that T. cruzi infection, as well as rP21, increases invasion and decreases intracellular proliferation of T. gondii in BeWo cells. The increase in invasion promoted by rP21 is dependent on its binding to CXCR4 and the actin cytoskeleton polymerization, while the decrease in proliferation is due to an arrest in the S/M phase in the parasite cell cycle, as well as interleukin (IL)-6 upregulation and IL-8 downmodulation. On the other hand, in human placental villi, rP21 can either increase or decrease T. gondii proliferation, whereas T. cruzi infection increases T. gondii proliferation. This increase can be explained by the induction of an anti-inflammatory environment through an increase in IL-4 and a decrease in IL-6, IL-8, macrophage migration inhibitory factor (MIF), and tumor necrosis factor (TNF)-α production. Discussion: In conclusion, in situations of coinfection, the presence of T. cruzi may favor the congenital transmission of T. gondii , highlighting the importance of neonatal screening for both diseases, as well as the importance of studies with P21 as a future therapeutic target for the treatment of Chagas disease, since it can also favor T. gondii infection. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (Copyright © 2023 de Souza, Teixeira, Fajardo Martínez, Silva, Luz, Lima Júnior, Rosini, dos Santos, de Oliveira, Paschoalino, Barbosa, Alves, Gomes, da Silva, Ferro and Barbosa.)
Databáze:	MEDLINE
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