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The Recombinant Form of Trypanosoma cruzi P21 Controls Infection by Modulating Host Immune Response.
Front Immunol. 2020; 11:1010.FI

Abstract

Trypanosoma cruzi P21 protein (P21) is a putative secreted and immunomodulatory molecule with potent bioactive properties such as induction of phagocytosis and actin cytoskeleton polymerization. Despite the bioactive properties described so far, the action of P21 on parasite replication in muscle cell lineage or T. cruzi parasitism during acute experimental infection is unclear. We observed that recombinant P21 (rP21) decreased the multiplication of T. cruzi in C2C12 myoblasts, phenomenon associated with greater actin polymerization and IFN-γ and IL-4 higher expression. During experimental infection, lower cardiac nests, inflammatory infiltrate and fibrosis were observed in mice infected and treated with rP21. These results were correlated with large expression of IFN-γ counterbalanced by high levels of IL-10, which was consistent with the lower cardiac tissue injury found in these mice. We have also observed that upon stress, such as that induced by the presence of the IFN-γ cytokine, T. cruzi produced more P21. The effect of P21 in controlling the replication of T. cruzi, may indicate an evolutionary mechanism of survival developed by the parasite. Thus, when subjected to different stress conditions, the protozoan produces more P21, which induces T. cruzi latency in the host organism, enabling the protozoan to evade the host's immune system.

Authors+Show Affiliations

Laboratório de Tripanosomatídeos, Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, Uberlândia, Brazil.Laboratório de Tripanosomatídeos, Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, Uberlândia, Brazil.Laboratório de Tripanosomatídeos, Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, Uberlândia, Brazil.Laboratório de Tripanosomatídeos, Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, Uberlândia, Brazil.Laboratório de Tripanosomatídeos, Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, Uberlândia, Brazil.Laboratório de Tripanosomatídeos, Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, Uberlândia, Brazil.Laboratório de Tripanosomatídeos, Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, Uberlândia, Brazil.Laboratório de Tripanosomatídeos, Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, Uberlândia, Brazil.Laboratório de Tripanosomatídeos, Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, Uberlândia, Brazil.Laboratório de Tripanosomatídeos, Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, Uberlândia, Brazil. Departamento de Microbiologia, Imunologia e Parasitologia, Universidade Federal de São Paulo, São Paulo, Brazil.Laboratório de Tripanosomatídeos, Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, Uberlândia, Brazil.Departamento de Microbiologia, Imunologia e Parasitologia, Universidade Federal de São Paulo, São Paulo, Brazil.Laboratório de Tripanosomatídeos, Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, Uberlândia, Brazil.Departamento de Microbiologia, Imunologia e Parasitologia, Universidade Federal do Triângulo Mineiro, Uberaba, Brazil.Departamento de Microbiologia, Imunologia e Parasitologia, Universidade Federal do Triângulo Mineiro, Uberaba, Brazil.Departamento de Anatomia Humana, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, Uberlândia, Brazil.Setor de Histologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, Uberlândia, Brazil.Departamento de Patologia, Genética e Evolução, Universidade Federal do Triangulo Mineiro, Uberaba, Brazil.Departamento de Microbiologia, Imunologia e Parasitologia, Universidade Federal do Triângulo Mineiro, Uberaba, Brazil.Departamento de Microbiologia, Imunologia e Parasitologia, Universidade Federal do Triângulo Mineiro, Uberaba, Brazil.Laboratório de Tripanosomatídeos, Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, Uberlândia, Brazil.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

32655546

Citation

Martins, Flávia Alves, et al. "The Recombinant Form of Trypanosoma Cruzi P21 Controls Infection By Modulating Host Immune Response." Frontiers in Immunology, vol. 11, 2020, p. 1010.
Martins FA, Dos Santos MA, Santos JG, et al. The Recombinant Form of Trypanosoma cruzi P21 Controls Infection by Modulating Host Immune Response. Front Immunol. 2020;11:1010.
Martins, F. A., Dos Santos, M. A., Santos, J. G., da Silva, A. A., Borges, B. C., da Costa, M. S., Tavares, P. C. B., Teixeira, S. C., Brígido, R. T. E. S., Teixeira, T. L., Rodrigues, C. C., Silva, N. S. L., de Oliveira, R. C., de Faria, L. C., Lemes, M. R., Zanon, R. G., Tomiosso, T. C., Machado, J. R., da Silva, M. V., ... da Silva, C. V. (2020). The Recombinant Form of Trypanosoma cruzi P21 Controls Infection by Modulating Host Immune Response. Frontiers in Immunology, 11, 1010. https://doi.org/10.3389/fimmu.2020.01010
Martins FA, et al. The Recombinant Form of Trypanosoma Cruzi P21 Controls Infection By Modulating Host Immune Response. Front Immunol. 2020;11:1010. PubMed PMID: 32655546.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The Recombinant Form of Trypanosoma cruzi P21 Controls Infection by Modulating Host Immune Response. AU - Martins,Flávia Alves, AU - Dos Santos,Marlus Alves, AU - Santos,Júlia de Gouveia, AU - da Silva,Aline Alves, AU - Borges,Bruna Cristina, AU - da Costa,Mylla Spirandelli, AU - Tavares,Paula Cristina Brígido, AU - Teixeira,Samuel Cota, AU - Brígido,Rebecca Tavares E Silva, AU - Teixeira,Thaise Lara, AU - Rodrigues,Cassiano Costa, AU - Silva,Nadjania Saraiva de Lira, AU - de Oliveira,Rayane Cristina, AU - de Faria,Laura Caroline, AU - Lemes,Marcela Rezende, AU - Zanon,Renata Graciele, AU - Tomiosso,Tatiana Carla, AU - Machado,Juliana Reis, AU - da Silva,Marcos Vinicius, AU - Oliveira,Carlo José Freire, AU - da Silva,Claudio Vieira, Y1 - 2020/06/05/ PY - 2020/02/29/received PY - 2020/04/28/accepted PY - 2020/7/14/entrez PY - 2020/7/14/pubmed PY - 2020/7/14/medline KW - Chagas disease KW - P21 KW - acute experimental infection KW - immune evasion KW - intracellular replication SP - 1010 EP - 1010 JF - Frontiers in immunology JO - Front Immunol VL - 11 N2 - Trypanosoma cruzi P21 protein (P21) is a putative secreted and immunomodulatory molecule with potent bioactive properties such as induction of phagocytosis and actin cytoskeleton polymerization. Despite the bioactive properties described so far, the action of P21 on parasite replication in muscle cell lineage or T. cruzi parasitism during acute experimental infection is unclear. We observed that recombinant P21 (rP21) decreased the multiplication of T. cruzi in C2C12 myoblasts, phenomenon associated with greater actin polymerization and IFN-γ and IL-4 higher expression. During experimental infection, lower cardiac nests, inflammatory infiltrate and fibrosis were observed in mice infected and treated with rP21. These results were correlated with large expression of IFN-γ counterbalanced by high levels of IL-10, which was consistent with the lower cardiac tissue injury found in these mice. We have also observed that upon stress, such as that induced by the presence of the IFN-γ cytokine, T. cruzi produced more P21. The effect of P21 in controlling the replication of T. cruzi, may indicate an evolutionary mechanism of survival developed by the parasite. Thus, when subjected to different stress conditions, the protozoan produces more P21, which induces T. cruzi latency in the host organism, enabling the protozoan to evade the host's immune system. SN - 1664-3224 UR - https://www.unboundmedicine.com/medline/citation/32655546/The_Recombinant_Form_of_Trypanosoma_cruzi_P21_Controls_Infection_by_Modulating_Host_Immune_Response L2 - https://doi.org/10.3389/fimmu.2020.01010 DB - PRIME DP - Unbound Medicine ER -
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