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. 2014 Feb 6;10:10. doi: 10.1186/1744-8069-10-10

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Copyright © 2014 Sauer et al.; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Hyperalgesia by TLR4 blockade in inflammatory pain. (A) Purified undifferentiated CD14⁺ human monocytes were incubated with 10 μg/ml LPS and a TLR4 inhibitor (TAK-242) in different doses. β-END release was quantified in the supernatant after 15 min (n = 6, * vs. LPS, *p <0.05, One Way RM ANOVA, Student-Newman-Keuls). (B, C) Rats with 4 d CFA inflammation were treated with TAK-242 i.pl. (1 μg, black triangle, and 10 μg, black square) and paw withdrawal latency (B) or paw pressure thresholds (C) were measured subsequently at indicated time points and compared to solvent (5% DMSO, black circle) in the inflamed paws (ipsilateral, ipsi). Paw pressure thresholds and paw withdrawal latencies from contralateral (contra, white symbols) paws are shown for comparison (n = 3–6, * vs. 0 min, * p < 0.05, Two way RM ANOVA, Student-Newman-Keuls). All data are presented as MEAN ± SEM.