ABC | Volume 110, Nº4, April 2018

Original Article Nascimento et al Vimentin and Anti Vimentin Antibodies in Chagas’ Disease Arq Bras Cardiol. 2018; 110(4):348-353 1. Calvet CM, Melo TG, Garzoni LR, Oliveira FO Jr, Neto DT, N S L M, et al. Current understanding of the Trypanosoma cruzi -cardiomyocyte interaction. Front Immunol. 2012 Oct 30;3:327. doi: 10.3389/fimmu.2012.00327. 2. Freire-de-Lima L, Fonseca LM, Oeltmann T, Mendonça-Previato L, Previato JO. The trans-sialidase, themajor Trypanosoma cruzi virulence factor: three decades of studies. Glycobiology. 2015;25(11):1142-9. doi: 10.1093/ glycob/cwv057. 3. Lowery J, Kuczmarski ER, Herrmann H, Goldman RD. 2015. Intermediate filaments play a pivotal role in regulating cell architecture and function. J Biol Chem. 2015;290(28):17145-53. doi: 10.1074/jbc.R115.640359. 4. Mahesh B. Leong HS, McCormack A, Sarathchandra P, Holder A, Rose ML. Autoantibodies to vimentin cause accelerated rejection of cardiac allografts. Am J Pathol. 2007;170(4):1415-27. doi: 10.2353/ajpath.2007.060728. 5. Azimzadeh AM, Pfeiffer S, Wu GS, Schröder C, Zhou H, Zorn GL 3 rd , et al. Humoral immunity to vimentin is associated with cardiac allograft injury in nonhuman primates. Am J Transplant . 2005;5(10):2349-59. doi: 10.1111/j.1600-6143.2005.01022.x. 6. Delunardo F, Scalzi V, Capozzi A, Camerini S, Misasi R, Pierdominici M, et al. Streptococcal-vimentincross-reactive antibodies induce microvascular cardiac endotelial pro inflammatory phenotype in rheumatic heart disease. Clin Exp Immunol. 2013;173(3):419-29. doi: 10.1111/cei.12135. 7. KaverinaI,RottnerK,SmallJV.Targeting,capture,andstabilizationofmicrotubules atearlyfocaladhesions.JCellBiol.1998;142(1):181-90.PMID:9660872. 8. Umezawa ES, Nascimento MS, Stolf AM. Enzyme-linked immunosorbent assay with Trypanosoma cruzi excreted-secreted antigens (TESA-ELISA) for serodiagnosis of acute and chronic Chagas disease. Diagn Microbiol Infect Dis. 2001;39(3):169-76. PMID: 11337184. References vimentin production is devoid of association with the parasite, which has no reactivity with anti-vimentin antibodies in any form. Viral infection alters host cell architecture similarly, as parvovirus in mice 10 but other pathogens also affects vimentin distribution in infected cells, with similar perivacuolar distribution, as in Salmonella infections. 11 Proteomics studies in experimental models of T.cruzi infection had shown higher plasma levels of vimentin related to disease severity, 12 which can offer to the immune response intracellular filaments for antibody production. Those data were expected as vimentin autoantibodies could be related to antigen exposure during active infection, as proposed in experimental models of T.cruzi infection. 12 Several other immune diseases that interact with cardiac muscle cells also presented anti-vimentin antibodies. Murine models of viral myocarditis presented those antibodies 13 and as well as post-streptococcal rheumatic fever patients 14 . Noninfectious myocarditis, as in coronary artery disease patients 15 and kidney or heart transplants recipients 16 also showed those antibodies resulted from any exposure of antigen, unregard the origin of cardiac muscle cell damage. Our data were similar to those findings and anti-vimentin antibodies induced during T.cruzi infection could be a marker of active disease in the host and its levels could also justify drug therapy in American Trypanosomiasis chronic infection, as a large group of asymptomatic or indeterminate patients would be submitted to treatment with frequent adverse reactions of the available drugs. Anti-vimentin antibodies could be a marker of cardiac muscle cell damage, appearing in American Trypanosomiasis patients during active muscle cell damage. Conclusions Our data revealed that anti-vimentin antibodies induced during activity of T. cruzi infection could be a marker of active disease in the host, despite absence of evident clinical involvement. This assay could be also a non-invasive follow‑up test during drug therapy in Chagas’ disease or American Trypanosomiasis. This test could allow the selection of possible active patients for therapy and also to supply a marker of disease activity after therapy, avoiding that a large group of asymptomatic patients without active disease were submitted to treatment with frequent adverse reactions. Anti-vimentin antibodies could be a marker of cardiac muscle cell inflammatory involvement, showed by American Trypanosomiasis patients with active muscle cell damage and must be tested in other cardiac muscle inflammatory conditions as viral myocarditis. Author contributions Conception and design of the research: Nascimento MS, Stolf AMS, Umezawa ES; Acquisition of data: Nascimento MS, Stolf MAS; Analysis and interpretation of the data: Nascimento MS, Stolf AMS, Andrade Junior HF, Pandey RP, Umezawa ES; Statistical analysis: Nascimento MS, Andrade Junior HF; Obtaining financing: Nascimento MS, Umezawa ES; Writing of the manuscript: Nascimento MS, Stolf AMS, Pandey RP; Critical revision of the manuscript for intellectual content: Nascimento MS, Andrade Junior HF, Pandey RP. Potential Conflict of Interest No potential conflict of interest relevant to this article was reported. Sources of Funding This study was funded by FMUSP. Study Association This article is part of the thesis of master submitted by Marilda Savoia Nascimento, from Universidade de São Paulo. Ethics approval and consent to participate This study was approved by the Ethics Committee of the Hospital das Clinicas da Universidade de São Paulo under the protocol number 0564/08. All the procedures in this study were in accordance with the 1975 Helsinki Declaration, updated in 2013. Informed consent was obtained from all participants included in the study. 352