Neuroimmune-Glia Interactions in the Sensory Ganglia Account for the Development of Acute Herpetic Neuralgia

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Silva, Jaqueline R. ; Lopes, Alexandre H. ; Talbot, Jhimmy ; Cecilio, Nerry T. ; Rossato, Mateus F. ; Silva, Rangel L. ; Souza, Guilherme R. ; Silva, Cassia R. ; Lucas, Guilherme ; Fonseca, Benedito A. ; Arruda, Eurico ; Alves-Filho, Jose C. ; Cunha, Fernando Q. ; Cunha, Thiago M.

• Document type: Journal article
• Source: JOURNAL OF NEUROSCIENCE; v. 37, n. 27, p. 6408-6422, JUL 5 2017.
• Web of Science Citations: 4

Abstract

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. (AU)

• FAPESP's process: 10/12309-8 - Role of the inflammatory immune response in the development of herpetic and post herpetic hypernociception
• Grantee: Jaqueline Raymondi Silva
• Support Opportunities: Scholarships in Brazil - Doctorate
• FAPESP's process: 13/08216-2 - CRID - Center for Research in Inflammatory Diseases
• Grantee: Fernando de Queiroz Cunha
• Support Opportunities: Research Grants - Research, Innovation and Dissemination Centers - RIDC
• FAPESP's process: 11/19670-0 - Mechanisms involved in the pathophysiology of rheumatoid arthritis, pain and sepsis
• Grantee: Fernando de Queiroz Cunha
• Support Opportunities: Research Projects - Thematic Grants