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Trigeminal Nociceptors Express TLR-4 and CD14: a Mechanism for Pain due to Infection

R. Wadachi1,2, and K.M. Hargreaves1,*

1 Department of Endodontics, UTHSCSA, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA; and
2 Department of Endodontics, Tokyo Medical and Dental University, Tokyo, Japan



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Figure 1. Evaluation of the expression patterns of TLR4 and CD14 in trigeminal sensory neurons. White arrows depict examples of neurons expressing both markers for each row of three images, and yellow arrows depict examples of neurons that express one but not both markers. Human trigeminal neurons were evaluated for co-localization of TLR4 (Panels A,D), CD14 (Panel J), with a marker for the capsaicin-sensitive subclass of nociceptors (TRPV1, Panels B,C for TLR4 and Panels K,L for CD14), or a marker of myelinated sensory neurons (N52, Panels E,F). Rat trigeminal neurons were evaluated for co-localization of TLR4 with TRPV1 (Panels G–I) and CD14 with TRPV1 (Panels M–O). The addition of blocking peptide or the deletion of primary or secondary antisera produced a complete loss of signal in both the human and rat tissues. Scale bar is 100 µm for Panels A–F and J–L, and 200 µm for Panels G–I and M–O.

 


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Figure 2. Evaluation of the expression patterns of TLR4 and CD14 in human coronal dental pulp. Normal control dental pulp was examined for expression of TLR4 (Panel A), CD14 (Panel B), and a marker of myelinated neurons (N52, Panel C). Inflamed dental pulp (defined as teeth with a response to thermal stimulation and having deep caries lesions) had two populations of TLR4 and CD14, with TLR4 (Panel D) or CD14 (Panel G) observed in round or stellate cells or in fibers coursing through coronal pulp. At least some of these fibers expressed N52 (TLR4, Panels E,F; CD14, Panels H,I). Exposure of inflamed pulp to only the secondary antibodies produced low background signal (Panels J,K). Scale bar is 100 µm.

 





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