DLK mediates the neuronal intrinsic immune response and regulates glial reaction and neuropathic pain
| Autor: | Kaili Liu, Wenwen Zeng, Zhongsheng Hu, Nan Deng |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Nervous system Sensory Receptor Cells Inflammation Mice 03 medical and health sciences 0302 clinical medicine Developmental Neuroscience medicine Animals Neuroinflammation Mice Knockout business.industry Nerve injury MAP Kinase Kinase Kinases medicine.disease Sensory neuron Astrogliosis Mice Inbred C57BL 030104 developmental biology medicine.anatomical_structure nervous system Neurology Neuropathic pain Neuralgia Sciatic nerve medicine.symptom business Neuroglia Neuroscience 030217 neurology & neurosurgery |
| Zdroj: | Experimental Neurology. 322:113056 |
| ISSN: | 0014-4886 |
| DOI: | 10.1016/j.expneurol.2019.113056 |
| Popis: | Inflammatory response triggered by nerve injury plays important roles in the development of neurological disorders, such as neuropathic pain. The signaling events leading to inflammation in the nervous system remain poorly understood. Here, by deleting Dlk in sensory neurons driven by Wnt1a-Cre, we show that dual leucine zipper kinase (DLK) is required for the neuronal intrinsic immune response to induce cytokines and chemokines such as Ccl2, Ccl7, and Ccl12 upon nerve injury. The DLK-controlled injury response in sensory neurons could regulate CD11b+ immune cell infiltration in the dorsal root ganglia, as well as microgliosis and astrogliosis in the spinal dorsal horn but not the ventral horn. Deficiency of Dlk drastically alleviates the neuropathic pain elicited by chronic constriction injury of the sciatic nerve. Thus, DLK is an essential component that mediates the neuronal intrinsic immune response to nerve injury in sensory neurons and regulates inflammation in the spinal cord. |
| Databáze: | OpenAIRE |
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