Investigation of the mechanisms by which antibody to VZV IE62 protein augments mechanical allodynia

急性疱疹性疼痛和疱疹后神经痛是顽固性神经源性疼痛，但其机制尚不清楚。我们之前发现，水痘带状疱疹病毒产生的一种即时早期蛋白IE62抗体的免疫反应，通过激活BDNF活性，增强了周围神经损伤小鼠的机械异位性疼痛。在本研究中，我们发现IE62抗体增加了小鼠急性疱疹性疼痛，并增加了向疱疹后神经痛的过渡。利用全局基因表达分析，我们发现脊髓半乳糖凝集素-3参与急性疱疹性异常性疼痛。然而，我们发现半乳糖凝集素-3不参与抗ie62抗体介导的机械异常性疼痛的增强。

Acute herpetic pain and postherpetic neuralgia are intractable neurogenic pain, however the mechanisms of the pain are still unknown. We previously found that immunoreaction to antibody to IE62, one of immediate early protein produced by varicella zoster virus, augment mechanical allodynia in mice with peripheral nerve injury via activation of BDNF activity. In this research, we found that antibody to IE62 augment the acute herpetic pain and increase the transition to postherpetic neuralgia in mice. Using global gene expression analysis, we revealed that spinal galectin-3 is involved in the acute herpetic allodynia. However, we found that galectin-3 is not involved in the anti-IE62 antibody-mediated augmentation of mechanical allodynia.