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Mediators of Inflammation
Volume 2010, Article ID 823486, 9 pages
Research Article

Inflammatory Role of Toll-Like Receptors in Human and Murine Adipose Tissue

1CNRS 8199-Institute of Biology, Pasteur Institute, 59019 Lille, France
2INSERM U859, IFR114 IMPRT, Faculté de Médecine, Pôle Recherche, 59045 Lille, France
3Department of Endocrinology, Clínica Universitaria de Navarra, Universitaria de Navarra, Univ. Navarra, and CIBER Fisiopatología de la Obesidad y Nutrición, Instituto de Salud Carlos III, 31008 Pamplona, Spain
4Genomic Medicine, Imperial College London, Hammersmith Hospital, Du Cane Road, London W12 0NN, UK

Received 19 October 2009; Accepted 7 January 2010

Academic Editor: Oreste Gualillo

Copyright © 2010 Odile Poulain-Godefroy 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.


It was recently demonstrated that TLR4 activation via dietary lipids triggers inflammatory pathway and alters insulin responsiveness in the fat tissue during obesity. Here, we question whether other TLR family members could participate in the TLR-mediated inflammatory processes occurring in the obese adipose tissue. We thus studied the expression of TLR1, TLR2, TLR4, and TLR6 in adipose tissue. These receptors are expressed in omental and subcutaneous human fat tissue, the expression being higher in the omental tissue, independently of the metabolic status of the subject. We demonstrated a correlation of TLRs expression within and between each depot suggesting a coregulation. Murine 3T3-L1 preadipocyte cells stimulated with Pam3CSK4 induced the expression of some proinflammatory markers. Therefore, beside TLR4, other toll-like receptors are differentially expressed in human fat tissue, and functional in an adipocyte cell line, suggesting that they might participate omental adipose tissue-related inflammation that occurs in obesity.