期刊
JOURNAL OF NEUROSCIENCE
卷 37, 期 27, 页码 6408-6422出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.2233-16.2017
关键词
glial cells; herpes; inflammation; pain
资金
- Sao Paulo Research Foundation (FAPESP) [2010/12309-8, 2011/19670-0, 2013/08216-2]
- University of Sao Paulo NAP-DIN [11.1.21625.01.0]
- European Union Seventh Framework Programme [HEALTH-F4-2011-281608 TIMER]
- International Association for the Study of Pain (Early Career Grant Award)
- FAPESP
- CNPq
Herpetic neuralgia is the most important symptom of herpes zoster disease, which is caused by Varicella zoster. Nevertheless, the pathophysiological mechanisms involved in herpetic neuralgia are not totally elucidated. Here, we examined the neuroimmune interactions at the sensory ganglia that account for the genesis of herpetic neuralgia using a murine model of Herpes Simplex Virus Type-1 (HSV-1) infection. The cutaneous HSV-1 infection of mice results in the development of a zosteriform-like skin lesion followed by a time-dependent increase in pain-like responses (mechanical allodynia). Leukocytes composed mainly of macrophages and neutrophils infiltrate infected DRGs and account for the development of herpetic neuralgia. Infiltrating leukocytes are responsible for driving the production of TNF, which in turn mediates the development of herpetic neuralgia through downregulation of the inwardly rectifying K+ channel Kir4.1 in satellite glial cells. These results revealed that neuroimmune-glia interactions at the sensory ganglia play a critical role in the genesis of herpetic neuralgia. In conclusion, the present study elucidates novel mechanisms involved in the genesis of acute herpetic pain and open new avenues for its control.
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