UMMS Affiliation

Department of Medicine, Division of Infectious Diseases and Immunology

Publication Date

6-26-2014

Document Type

Article

Subjects

Animals; CD8-Positive T-Lymphocytes; Chagas Disease; Female; Glycoproteins; Interleukin-12; Male; Mice; Mice, Inbred BALB C; Neuraminidase; Trypanosoma cruzi

Disciplines

Genetics and Genomics | Immunology and Infectious Disease | Immunoprophylaxis and Therapy | Parasitic Diseases | Parasitology

Abstract

In earlier studies, we reported that a heterologous prime-boost regimen using recombinant plasmid DNA followed by replication-defective adenovirus vector, both containing Trypanosoma cruzi genes encoding trans-sialidase (TS) and amastigote surface protein (ASP) 2, provided protective immunity against experimental infection with a reticulotropic strain of this human protozoan parasite. Herein, we tested the outcome of genetic vaccination of F1 (CB10XBALB/c) mice challenged with myotropic parasite strains (Brazil and Colombian). Initially, we determined that the coadministration during priming of a DNA plasmid containing the murine IL-12 gene improved the immune response and was essential for protective immunity elicited by the heterologous prime-boost regimen in susceptible male mice against acute lethal infections with these parasites. The prophylactic or therapeutic vaccination of resistant female mice led to a drastic reduction in the number of inflammatory infiltrates in cardiac and skeletal muscles during the chronic phase of infection with either strain. Analysis of the electrocardiographic parameters showed that prophylactic vaccination reduced the frequencies of sinus arrhythmia and atrioventricular block. Our results confirmed that prophylactic vaccination using the TS and ASP-2 genes benefits the host against acute and chronic pathologies caused by T. cruzi and should be further evaluated for the development of a veterinary or human vaccine against Chagas disease.

Rights and Permissions

Citation: Mediators Inflamm. 2014;2014:605023. doi: 10.1155/2014/605023. Epub 2014 Jun 26. Link to article on publisher's site

DOI of Published Version

10.1155/2014/605023

Comments

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Related Resources

Link to Article in PubMed

Journal/Book/Conference Title

Mediators of inflammation

PubMed ID

25061263

Creative Commons License

Creative Commons Attribution 3.0 License
This work is licensed under a Creative Commons Attribution 3.0 License.

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