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Reports from Fiocruz Add New Data to Findings in Monoclonal Antibodies (Tumor Necrosis Factor Is a Therapeutic Target for Immunological Unbalance and...

September 10, 2014



Reports from Fiocruz Add New Data to Findings in Monoclonal Antibodies (Tumor Necrosis Factor Is a Therapeutic Target for Immunological Unbalance and Cardiac Abnormalities in Chronic Experimental Chagas' Heart Disease)

By a News Reporter-Staff News Editor at Biotech Week -- New research on Drugs and Therapies is the subject of a report. According to news originating from Rio de Janeiro, Brazil, by NewsRx correspondents, research stated, "Chagas disease (CD) is characterized by parasite persistence and immunological unbalance favoring systemic inflammatory profile. Chronic chagasic cardiomyopathy, the main manifestation of CD, occurs in a TNF-enriched milieu and frequently progresses to heart failure."

Our news journalists obtained a quote from the research from Fiocruz, "Aim of the Study. To challenge the hypothesis that TNF plays a key role in Trypanosoma cruzi-induced immune deregulation and cardiac abnormalities, we tested the effect of the anti-TNF antibody Infliximab in chronically T. cruzi-infected C57BL/6 mice, a model with immunological, electrical, and histopathological abnormalities resembling Chagas' heart disease. Infliximab therapy did not reactivate parasite but reshaped the immune response as reduced TNF mRNA expression in the cardiac tissue and plasma TNF and IFN gamma levels; diminished the frequency of IL-17A(+) but increased IL-10(+) CD4(+) T-cells; reduced TNF+ but augmented IL-10(+) Ly6C(+) and F4/80(+) cells. Further, anti-TNF therapy decreased cytotoxic activity but preserved IFN gamma-producing VNHRFTLV-specific CD8(+) T-cells in spleen and reduced the number of perforin(+) cells infiltrating the myocardium. Importantly, Infliximab reduced the frequency of mice afflicted by arrhythmias and second degree atrioventricular blocks and decreased fibronectin deposition in the cardiac tissue."

According to the news editors, the research concluded: "Our data support that TNF is a crucial player in the pathogenesis of Chagas' heart disease fueling immunological unbalance which contributes to cardiac abnormalities."

For more information on this research see: Tumor Necrosis Factor Is a Therapeutic Target for Immunological Unbalance and Cardiac Abnormalities in Chronic Experimental Chagas' Heart Disease. Mediators of Inflammation, 2014;():1-16. Mediators of Inflammation can be contacted at: Hindawi Publishing Corporation, 410 Park Avenue, 15TH Floor, #287 Pmb, New York, NY 10022, USA. (Hindawi Publishing - www.hindawi.com; Mediators of Inflammation - www.hindawi.com/journals/mi/)

The news correspondents report that additional information may be obtained from I.R. Pereira, Fiocruz MS, IOC, Lab Biol Mol & Doencas Endem, BR-21045900 Rio De Janeiro, RJ, Brazil. Additional authors for this research include G. Vilar-Pereira, A.A. Silva, O.C. Moreira, C. Britto, E.D.M. Sarmento and J. Lannes-Vieira (see also Drugs and Therapies).

Keywords for this news article include: Rio de Janeiro, Brazil, South America, Antirheumatics, Cytokines, Drugs, Drugs and Therapies, Immunologic Agents, Infliximab, Intercellular Signaling Peptides and Proteins, Monoclonal Antibodies, Therapy, Tumor Necrosis Factor (TNF) Inhibitors, Tumor Necrosis Factors

Our reports deliver fact-based news of research and discoveries from around the world. Copyright 2014, NewsRx LLC


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Source: Biotech Week


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