dc.contributor.author | Colas, RA | en_US |
dc.contributor.author | Ashton, AW | en_US |
dc.contributor.author | Mukherjee, S | en_US |
dc.contributor.author | Dalli, J | en_US |
dc.contributor.author | Akide-Ndunge, OB | en_US |
dc.contributor.author | Huang, H | en_US |
dc.contributor.author | Desruisseaux, MS | en_US |
dc.contributor.author | Guan, F | en_US |
dc.contributor.author | Jelicks, LA | en_US |
dc.contributor.author | Matos Dos Santos, F | en_US |
dc.contributor.author | Nagajyothi, J | en_US |
dc.contributor.author | Zingman, MA | en_US |
dc.contributor.author | Reyes, J | en_US |
dc.contributor.author | Weiss, LM | en_US |
dc.contributor.author | Serhan, CN | en_US |
dc.contributor.author | Tanowitz, HB | en_US |
dc.date.accessioned | 2018-11-13T09:00:58Z | |
dc.date.available | 2018-01-22 | en_US |
dc.date.issued | 2018-04 | en_US |
dc.date.submitted | 2018-04-07T09:27:51.580Z | |
dc.identifier.uri | http://qmro.qmul.ac.uk/xmlui/handle/123456789/50043 | |
dc.description.abstract | Trypanosoma cruzi is a protozoan parasite that causes Chagas disease (CD). CD is a persistent, lifelong infection affecting many organs, most notably the heart, where it may result in acute myocarditis and chronic cardiomyopathy. The pathological features include myocardial inflammation and fibrosis. In the Brazil strain-infected CD-1 mouse, which recapitulates many of the features of human infection, we found increased plasma levels of resolvin D1 (RvD1), a specialized proresolving mediator of inflammation, during both the acute and chronic phases of infection (>100 days postinfection) as determined by enzyme-linked immunosorbent assay (ELISA). Additionally, ELISA on lysates of trypomastigotes of both strains Tulahuen and Brazil revealed elevated levels of RvD1 compared with lysates of cultured epimastigotes of T. cruzi, tachyzoites of Toxoplasma gondii, trypomastigotes of Trypanosoma brucei, cultured L6E9 myoblasts, and culture medium containing no cells. Lysates of T. cruzi-infected myoblasts also displayed increased levels of RvD1. Lipid mediator metabolomics confirmed that the trypomastigotes of T. cruzi produced RvD1, RvD5, and RvE2, which have been demonstrated to modulate the host response to bacterial infections. Plasma RvD1 levels may be both host and parasite derived. Since T. cruzi synthesizes specialized proresolving mediators of inflammation, as well as proinflammatory eicosanoids, such as thromboxane A2, one may speculate that by using these lipid mediators to modulate its microenvironment, the parasite is able to survive. | en_US |
dc.description.sponsorship | This work was supported by NIH Grants PO1 GM095467(CNS) and AI-214000 (HBT) | en_US |
dc.language | eng | en_US |
dc.language.iso | en | en_US |
dc.relation.ispartof | Infect Immun | en_US |
dc.subject | Chagas disease | en_US |
dc.subject | Trypanosoma cruzi | en_US |
dc.subject | eicosanoids | en_US |
dc.subject | host-parasite relationship | en_US |
dc.subject | immune modulation | en_US |
dc.subject | inflammation | en_US |
dc.subject | resolvin | en_US |
dc.subject | resolvin D1 | en_US |
dc.subject | resolvin D5 | en_US |
dc.subject | resolvin E2 | en_US |
dc.subject | resolvins | en_US |
dc.subject | Biomarkers | en_US |
dc.subject | Cardiac Imaging Techniques | en_US |
dc.subject | Chagas Disease | en_US |
dc.subject | Chromatography, Liquid | en_US |
dc.subject | Docosahexaenoic Acids | en_US |
dc.subject | Eicosapentaenoic Acid | en_US |
dc.subject | Host-Parasite Interactions | en_US |
dc.subject | Immunomodulation | en_US |
dc.subject | Lipid Metabolism | en_US |
dc.subject | Metabolome | en_US |
dc.subject | Prostaglandins | en_US |
dc.subject | Tandem Mass Spectrometry | en_US |
dc.subject | Trypanosoma cruzi | en_US |
dc.title | Trypanosoma cruzi Produces the Specialized Proresolving Mediators Resolvin D1, Resolvin D5, and Resolvin E2. | en_US |
dc.type | Article | |
dc.rights.holder | Copyright © 2018 American Society for Microbiology. All Rights Reserved. | |
dc.identifier.doi | 10.1128/IAI.00688-17 | en_US |
pubs.author-url | https://www.ncbi.nlm.nih.gov/pubmed/29358332 | en_US |
pubs.issue | 4 | en_US |
pubs.notes | Not known | en_US |
pubs.publication-status | Published online | en_US |
pubs.volume | 86 | en_US |
dcterms.dateAccepted | 2018-01-14 | en_US |