Plasma Cytokine Profile in Tropical Endomyocardial Fibrosis: Predominance of TNF-a, IL-4 and IL-10

Plasma Cytokine Profile in Tropical Endomyocardial Fibrosis: Predominance of TNF-a, IL-4 and IL-10

Author Bossa, Aline S. Google Scholar
Salemi, Vera M. C. Google Scholar
Ribeiro, Susan P. Google Scholar
Rosa, Daniela Santoro Autor UNIFESP Google Scholar
Pinto Ferreira, Ludmila Rodrigues Google Scholar
Ferreira, Suzete C. Google Scholar
Nishiya, Anna Shoko Google Scholar
Mady, Charles Google Scholar
Kalil, Jorge Google Scholar
Cunha-Neto, Edecio Google Scholar
Institution Universidade de São Paulo (USP)
ProSangue Fdn
Inst Investigat Immunol
Universidade Federal de São Paulo (UNIFESP)
Abstract Background: the participation of immune/inflammatory mechanisms in the pathogenesis of tropical endomyocardial fibrosis (EMF) has been suggested by the finding of early blood and myocardial eosinophilia. However, the inflammatory activation status of late-stage EMF patients is still unknown.Methodology/Principal findings: We evaluated pro- and anti-inflammatory cytokine levels in plasma samples from late stage EMF patients. Cytokine levels of Tumor Necrosis Factor (TNF)-alpha, Interferon (IFN)-gamma, Interleukin (IL)-2, IL-4, IL-6, and IL-10 were assayed in plasma samples from 27 EMF patients and compared with those of healthy control subjects. All EMF patients displayed detectable plasma levels of at least one of the cytokines tested. We found that TNF-alpha, IL-6, IL-4, and IL-10 were each detected in at least 74% of tested sera, and plasma levels of IL-10, IL-4, and TNF-alpha were significantly higher than those of controls. Plasma levels of such cytokines positively correlated with each other.Conclusions/Significance: the mixed pro-and anti-inflammatory/Th2circulating cytokine profile in EMF is consistent with the presence of a persistent inflammatory stimulus. On the other hand, the detection of increased levels of TNF-alpha may be secondary to the cardiovascular involvement observed in these patients, whereas IL-4 and IL-10 may have been upregulated as a homeostatic mechanism to buffer both production and deleterious cardiovascular effects of pro-inflammatory cytokines. Further studies might establish whether these findings play a role in disease pathogenesis.
Language English
Sponsor Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Date 2014-10-10
Published in Plos One. San Francisco: Public Library Science, v. 9, n. 10, 5 p., 2014.
ISSN 1932-6203 (Sherpa/Romeo, impact factor)
Publisher Public Library Science
Extent 5
Access rights Open access Open Access
Type Article
Web of Science ID WOS:000343730400039

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