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Publications

Journal Article Research Support, Non-U.S. Gov't Epublish 10 citations

PubMed: 37915581 DOI: 10.3389/fimmu.2023.1243480

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

Front Immunol 14:1243480

Authors: Guilherme de Souza, Samuel Cota Teixeira, Aryani Felixa Fajardo Martínez, Rafaela José Silva, Luana Carvalho Luz, Joed Pires de Lima Júnior, Alessandra Monteiro Rosini, Natália Carine Lima Dos Santos, Rafael Martins de Oliveira, Marina Paschoalino, Matheus Carvalho Barbosa, Rosiane Nascimento Alves, Angelica Oliveira Gomes, Claudio Vieira da Silva, Eloisa Amália Vieira Ferro, Bellisa Freitas Barbosa

Affiliations

  • Laboratory of Immunophysiology of Reproduction, Institute of Biomedical Sciences, Universidade Federal de Uberlândia, Uberlândia, MG, Brazil.
  • Department of Agricultural and Natural Science, Universidade do Estado de Minas Gerais, Ituiutaba, MG, Brazil.
  • Institute of Natural and Biological Sciences, Universidade Federal do Triângulo Mineiro, Uberaba, MG, Brazil.
  • Laboratory of Trypanosomatids, Institute of Biomedical Sciences, Universidade Federal de Uberlândia, Uberlândia, Brazil.

Abstract

Introduction

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 , the etiologic agent of Chagas disease, as well as one of its proteins, P21, could aggravate infection.

Methods

In this sense, we aimed to investigate the impact of and recombinant P21 (rP21) on infection in BeWo cells and human placental explants.

Results

Our results showed that infection, as well as rP21, increases invasion and decreases intracellular proliferation of 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 proliferation, whereas infection increases 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 may favor the congenital transmission of , 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 infection.

MeSH

Toxoplasmosis, Congenital, Cells, Coinfection, Immune System Diseases, Therapeutics, Chagas Disease, Infections, Recombinant Proteins

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