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.

• Tipo de documento: Artigo Científico
• Fonte: JOURNAL OF NEUROSCIENCE; v. 37, n. 27, p. 6408-6422, JUL 5 2017.
• Citações Web of Science: 4

Resumo

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)

• Processo FAPESP: 10/12309-8 - Papel da resposta imune inflamatória no desenvolvimento da hipernocicepção herpética e pós-herpética
• Beneficiário: Jaqueline Raymondi Silva
• Modalidade de apoio: Bolsas no Brasil - Doutorado
• Processo FAPESP: 13/08216-2 - CPDI - Centro de Pesquisa em Doenças Inflamatórias
• Beneficiário: Fernando de Queiroz Cunha
• Modalidade de apoio: Auxílio à Pesquisa - Centros de Pesquisa, Inovação e Difusão - CEPIDs
• Processo FAPESP: 11/19670-0 - Mecanismos envolvidos na fisiopatologia da artrite reumatóide, dor e sepse
• Beneficiário: Fernando de Queiroz Cunha
• Modalidade de apoio: Auxílio à Pesquisa - Temático