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Mediators of Inflammation
Volume 2014 (2014), Article ID 479395, 11 pages
Research Article

TLR4-Mediated Blunting of Inflammatory Responses to Eccentric Exercise in Young Women

1Institute of Biomedicine (IBIOMED), University of León, Campus Universitario, 24071 León, Spain
2Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm 171 77, Sweden

Received 4 June 2014; Revised 9 August 2014; Accepted 10 August 2014; Published 9 September 2014

Academic Editor: Fulvio D'Acquisto

Copyright © 2014 Rodrigo Fernandez-Gonzalo et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


This study assessed the inflammatory response mediated by the toll-like receptor 4 (TLR4) signaling pathway after acute eccentric exercise before and after an eccentric training program in women. Twenty women performed two acute eccentric bouts using a squat machine over a ~9 week interval. The training group (TG) carried out an eccentric training program during 6 weeks, while the control group (CG) did not follow any training. Protein content of markers involved in the TLR4-mediated activation of several nuclear transcription factors, such as nuclear factor κB (NF-κB), and interferon regulatory transcription factor 3 (IRF3), was analyzed. The inflammatory response after the first acute bout was similar between TG and CG, showing an upregulation of all the markers analyzed, with the exception of IRF3. After the second bout, the upregulation of TLR4 signaling pathway was blunted in TG, but not in CG, through both the myeloid differentiation factor 88- and toll/interleukin-1 receptor domain containing adapter inducing interferon-β-dependent pathways. These results highlight the role of the TLR4 in controlling the exercise-induced inflammatory response in young women. More importantly, these data suggest eccentric training may help to prevent TLR4 activation principally through NF-κB, and perhaps IRF3, downstream signaling in this population.