2020
DOI: 10.3390/vaccines8010096
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Antigen-Based Nano-Immunotherapy Controls Parasite Persistence, Inflammatory and Oxidative Stress, and Cardiac Fibrosis, the Hallmarks of Chronic Chagas Cardiomyopathy, in A Mouse Model of Trypanosoma cruzi Infection

Abstract: Chagas cardiomyopathy is caused by Trypanosoma cruzi (Tc). We identified two candidate antigens (TcG2 and TcG4) that elicit antibodies and T cell responses in naturally infected diverse hosts. In this study, we cloned TcG2 and TcG4 in a nanovector and evaluated whether nano-immunotherapy (referred as nano2/4) offers resistance to chronic Chagas disease. For this, C57BL/6 mice were infected with Tc and given nano2/4 at 21 and 42 days post-infection (pi). Non-infected, infected, and infected mice treated with pc… Show more

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Cited by 13 publications
(13 citation statements)
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References 49 publications
(66 reference statements)
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“…A variety of alterations in the interstitial myocardial collagen network, macrophages, CMs, CFs, ECs and vascular cells are closely linked with fibrillar alteration in the heart. At the molecular and cellular levels, cardiovascular fibrosis is linked with reduced nitric oxide release, increased ROS generation, the activation of transcription factors, the stimulation of proinflammatory and profibrotic pathways, increased collagen deposition and ECM remodeling [1,3,[28][29][30][31]. Inflammation and oxidative stress seem to be positively associated with remodeling processes, ultimately contributing to cardiac dilation and dysfunction [13,29].…”
Section: Mir-122 and Cardiovascular Fibrosis And Remodelingmentioning
confidence: 99%
See 1 more Smart Citation
“…A variety of alterations in the interstitial myocardial collagen network, macrophages, CMs, CFs, ECs and vascular cells are closely linked with fibrillar alteration in the heart. At the molecular and cellular levels, cardiovascular fibrosis is linked with reduced nitric oxide release, increased ROS generation, the activation of transcription factors, the stimulation of proinflammatory and profibrotic pathways, increased collagen deposition and ECM remodeling [1,3,[28][29][30][31]. Inflammation and oxidative stress seem to be positively associated with remodeling processes, ultimately contributing to cardiac dilation and dysfunction [13,29].…”
Section: Mir-122 and Cardiovascular Fibrosis And Remodelingmentioning
confidence: 99%
“…Inflammation and oxidative stress seem to be positively associated with remodeling processes, ultimately contributing to cardiac dilation and dysfunction [ 13 , 29 ]. MiRs participate in regulating cell proliferation, migration, differentiation, and apoptosis and function as crucial determinants and biomarkers of cardiovascular fibrosis [ 1 , 5 , 6 , 30 , 32 ]. In particular, miR-122 has been implicated in the progression of fibrosis and acts as a circulatory biomarker in hypertension and HF [ 1 , 6 , 17 , 18 , 33 37 ].…”
Section: Mir-122 and Cardiovascular Fibrosis And Remodelingmentioning
confidence: 99%
“…The fulllength cDNAs for the two antigens were previously cloned into pCDNA3.1 eukaryotic expression plasmid and the recombinant plasmids were purified by anion exchange chromatography by using a Qiagen Endo-free maxi prep kit (Qiagen, Chatsworth, CA) (9, 10). A CMV promoter-based NTC9385R-MCS nanoplasmid (Nature technology, Lincoln, NE) was utilized for sub-cloning the full-length genes encoding for TcG2 and TcG4 (18). The recombinant nanoplasmids NTC9385R-TcG2 and NTC9385R-TcG4 were sequenced to confirm the orientation and open reading frame, and purified by using the HyperGRO fermentation process (18).…”
Section: Vaccine Constructsmentioning
confidence: 99%
“…A CMV promoter-based NTC9385R-MCS nanoplasmid (Nature technology, Lincoln, NE) was utilized for sub-cloning the full-length genes encoding for TcG2 and TcG4 (18). The recombinant nanoplasmids NTC9385R-TcG2 and NTC9385R-TcG4 were sequenced to confirm the orientation and open reading frame, and purified by using the HyperGRO fermentation process (18).…”
Section: Vaccine Constructsmentioning
confidence: 99%
See 1 more Smart Citation