Experimental evidences that P21 protein controls Trypanosoma cruzi replication and modulates the pathogenesis of infection

P21 is a protein secreted by Trypanosoma cruzi (T. cruzi). Previous studies have shown a spectrum of biological activities performed by P21 such as induction of phagocytosis, leukocyte chemotaxis and inhibition of angiogenesis. However, the activity of P21 in T. cruzi infection remains unknown. Here...

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Published in:	Microbial pathogenesis Vol. 135; p. 103618
Main Authors:	Teixeira, Thaise L., Castilhos, Patrícia, Rodrigues, Cassiano C., da Silva, Aline A., Brígido, Rebecca TS, Teixeira, Samuel C., Borges, Bruna C., Dos Santos, Marlus A., Martins, Flávia A., Santos, Paulo César F., Servato, João Paulo S., Silva, M.S., da Silva, M.J.B., Elias, M.C., da Silva, Claudio V.
Format:	Journal Article
Language:	English
Published:	England Elsevier Ltd 01-10-2019
Subjects:	Angiogenesis Chagas disease Fibrosis Intracellular replication Life cycle P21 protein Chagas disease P21 protein Angiogenesis Life cycle Intracellular replication Fibrosis
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Summary:	P21 is a protein secreted by Trypanosoma cruzi (T. cruzi). Previous studies have shown a spectrum of biological activities performed by P21 such as induction of phagocytosis, leukocyte chemotaxis and inhibition of angiogenesis. However, the activity of P21 in T. cruzi infection remains unknown. Here, we reported the role of P21 in mice harboring late T. cruzi infection. Treatment with recombinant P21 protein (rP21) reduced parasite load and angiogenesis, and induced fibrosis in the cardiac tissue of infected mice. In addition, rP21 reduced the growth of epimastigotes, inhibited intracellular replication of amastigotes and modulated the parasite cell cycle. Our data suggest that P21 controls parasite replication in the host, supporting the survival of both parasite and host. [Display omitted] •T. cruzi P21 plays important role in Chagas disease pathogenesis.•T. cruzi P21 controls parasite intracellular multiplication.•T. cruzi P21 activities leads infection to the chronic phase.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0882-4010 1096-1208
DOI:	10.1016/j.micpath.2019.103618