TY - JOUR ID - 8250 TI - Up-regulation of TLR2 and TLR4 in high mobility group Box1-stimulated macrophages in pulpitis patients JO - Iranian Journal of Basic Medical Sciences JA - IJBMS LA - en SN - 2008-3866 AU - Mahmoudi, Javad AU - Sabermarouf, Babak AU - Baradaran, Behzad AU - Sadat-Hatamnezhad, Leila AU - Sandoghchian Shotorbani, Siamak AD - Neurosciences Research Center, Tabriz University of Medical Science, Tabriz, Iran AD - Immunology Research Center, Tabriz University of Medical Science, Tabriz, Iran AD - Department of Immunology, Tabriz Branch, Islamic Azad University, Tabriz, Iran Y1 - 2017 PY - 2017 VL - 20 IS - 2 SP - 209 EP - 215 KW - HMGB1 KW - Pulpitis KW - TLR2 KW - TLR4 DO - 10.22038/ijbms.2017.8250 N2 - Objective(s): High Mobility Group Box1 (HMGB1) is a nonhistone, DNA-binding protein that serves a crucial role in regulating gene transcription and is involved in a variety of proinflammatory, extracellular activities. The aim of this study was to explore whether HMGB1 stimulation can up-regulate the expression of Toll-like Receptor 2 (TLR2) and Toll-like Receptor 4 (TLR4) on macrophages from pulpitis and to clarify the subsequent events involving Th17 cells and Th17 cell-associated cytokine changes. Materials and Methods: Having prepared dental pulp tissues of pulpitis and healthy controls, macrophage were isolated and cultured. Macrophages were thereafter stimulated by HMGB1 time course. RT-QPCR, flowcytometer, immunofluorescence, Western blotting, and ELISA techniques were used in the present research. Results: Our results showed that the expression of TLR2 and TLR4 on macrophages stimulated with HMGB1 increased in pulpitis compared with controls (macrophages without HMGB1 stimulation) with a statistical significance (P<0.001). In addition, the levels of IL-17, IL-23, and IL-6 in supernatants from cultured macrophages stimulated with HMGB1 from pulpitis increased, and NF-kB, the downstream target of TLR2 and TLR4, also showed a marked elevation after macrophages’ stimulation by HMGB1. Conclusion: The evidence from the present study suggests that the enhanced TLR2 and TLR4 pathways and Th17 cell polarization may be due to HMGB1 stimulation in pulpitis. UR - https://ijbms.mums.ac.ir/article_8250.html L1 - https://ijbms.mums.ac.ir/article_8250_3b98ce9154b9aecf3ce2d86fb6b01e14.pdf ER -