Macrophages in trigeminal ganglion contribute to ectopic mechanical hypersensitivity following inferior alveolar nerve injury in rats.
Macrophages in trigeminal ganglion contribute to ectopic mechanical hypersensitivity following inferior alveolar nerve injury in rats.
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DOI：
10.1186/s12974-017-1022-3
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发表时间：
2017-12-16
影响因子：
9.3
通讯作者：
Iwata K
中科院分区：
文献类型：
--
作者：
Batbold D;Shinoda M;Honda K;Furukawa A;Koizumi M;Akasaka R;Yamaguchi S;Iwata K
在拔牙或种植过程中，可能会发生意外的下颌神经损伤，导致异位口面部疼痛。下颌神经损伤后异位口面部疼痛的确切机制尚不清楚。在这里，我们研究了巨噬细胞和肿瘤坏死因子α在三叉神经节在下牙槽神经切断后异位口面部疼痛中的作用。行IANX检查，连续15d测定IANX同侧须垫皮肤的机械性头部撤除阈值(MHWT)。在IANX后第3天检测Iba1在TG中的表达，并连续神经节内注射巨噬细胞去除剂Cloposome-A(LCCA)，测量IANX同侧须垫皮肤的MHWT。免疫组织化学方法检测Tg内肿瘤坏死因子α受体1(TnFR1I)免疫反应阳性细胞的表达，Tg中肿瘤坏死因子受体1(TnFR1IR)免疫反应细胞的表达。IANX后15d，Tg中MHWT显著减少，IANX后3d，Tg中Iba1-IR细胞明显增多。连续神经节内注射巨噬细胞去除剂LCCA可显著减少TG中IBA1-IR细胞的数量，并逆转IANX引起的须垫皮肤MHWT的下降。肿瘤坏死因子α在缺血后第3天在三叉神经节表达增加，连续神经节内注射肿瘤坏死因子α抑制剂依那西普后，其表达降低。依那西普也能恢复MHWT的下降，在IANX后第3天，TG中的TNFR1-IR细胞增加。这些发现提示，三叉神经节内的巨噬细胞产生肿瘤坏死因子α所产生的信号级联反应是导致IANX后胡须垫皮肤异位机械性痛觉过敏的原因。
Accidental mandibular nerve injury may occur during tooth extraction or implant procedures, causing ectopic orofacial pain. The exact mechanisms underlying ectopic orofacial pain following mandibular nerve injury is still unknown. Here, we investigated the role of macrophages and tumor necrosis factor alpha (TNFα) in the trigeminal ganglion (TG) in ectopic orofacial pain following inferior alveolar nerve transection (IANX). IANX was performed and the mechanical head-withdrawal threshold (MHWT) in the whisker pad skin ipsilateral to IANX was measured for 15 days. Expression of Iba1 in the TG was examined on day 3 after IANX, and the MHWT in the whisker pad skin ipsilateral to IANX was measured following successive intra-ganglion administration of the macrophage depletion agent liposomal clodronate Clophosome-A (LCCA). TNFα expression in the TG and the MHWT in the whisker pad skin ipsilateral to IANX following successive intra-ganglion administration of the TNFα blocker etanercept were measured on day 3 after IANX, and tumor necrosis factor receptor-1 (TNFR1) immunoreactive (IR) cells in the TG were analyzed immunohistochemically on day 3. The MHWT in the whisker pad skin was significantly decreased for 15 days, and the number of Iba1-IR cells was significantly increased in the TG on day 3 after IANX. Successive intra-ganglion administration of the macrophage depletion agent LCCA significantly reduced the increased number of Iba1-IR cells in the TG and reversed the IANX-induced decrease in MHWT in the whisker pad skin. TNFα expression was increased in the TG on day 3 after IANX and was reduced following successive intra-ganglion administration of the TNFα inhibitor etanercept. The decreased MHWT was also recovered by etanercept administration, and TNFR1-IR cells in the TG were increased on day 3 following IANX. These findings suggest that signaling cascades resulting from the production of TNFα by infiltrated macrophages in the TG contributes to the development of ectopic mechanical allodynia in whisker pad skin following IANX.
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影响因子：
3.3
作者：
Kaji K;Shinoda M;Honda K;Unno S;Shimizu N;Iwata K
通讯作者：
Iwata K
影响因子：
3.3
作者：
Kim D;You B;Lim H;Lee SJ
通讯作者：
Lee SJ
DOI：
10.1523/jneurosci.3992-08.2009
发表时间：
2009-03-25
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Gensel JC;Nakamura S;Guan Z;van Rooijen N;Ankeny DP;Popovich PG
通讯作者：
Popovich PG
影响因子：
4.6
作者：
Leo M;Argalski S;Schäfers M;Hagenacker T
通讯作者：
Hagenacker T
影响因子：
3.3
作者：
Katagiri A;Shinoda M;Honda K;Toyofuku A;Sessle BJ;Iwata K
通讯作者：
Iwata K