| Full text | |
| Author(s): Show less - |
Silva, Cassia R.
[1, 2]
;
Melo, Bruno M. S.
[1]
;
Silva, Jaqueline R.
[1]
;
Lopes, Alexandre H.
[1]
;
Pereira, Janaina A.
[1]
;
Cecilio, Nerry T.
[1]
;
Berlink, Jonilson
[1, 3]
;
Souza, Giovani G.
[1]
;
Lucas, Guilherme
[4]
;
Vogl, Thomas
[5]
;
Cunha, Fernando Q.
[1]
;
Alves-Filho, Jose C.
[1]
;
Cunha, Thiago M.
[1]
Total Authors: 13
|
| Affiliation: | [1] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Pharmacol, Ctr Res Inflammatory Dis CRID, Ribeirao Preto, SP - Brazil
[2] Univ Fed Uberlandia, Inst Biotechnol, Grad Program Genet & Biochem, BR-38408100 Uberlandia, MG - Brazil
[3] Fed Univ Western Bahia, Ctr Biol & Hlth Sci, Barreiras, BA - Brazil
[4] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Physiol, Ribeirao Preto - Brazil
[5] Univ Munster, Inst Immunol, D-48149 Munster - Germany
Total Affiliations: 5
|
| Document type: | Journal article |
| Source: | BRAIN BEHAVIOR AND IMMUNITY; v. 88, p. 353-362, AUG 2020. |
| Web of Science Citations: | 0 |
| Abstract | |
Herpetic neuralgia is a painful condition following herpes zoster disease, which results from Varicella-zoster virus reactivation in the dorsal or trigeminal sensory ganglia. Nevertheless, the pathophysiological mechanisms involved in herpetic neuralgia are not well understood. Recently, we identified, that neuroimmune-glia interactions in the sensory ganglion is a critical mechanism for the development of herpetic neuralgia. Here, we investigate the contribution of S100A9, a well-known pro-inflammatory molecule produced by myeloid cells, for the development of herpetic neuralgia using a murine model of HSV-1 infection. We found that cutaneous HSV-1 infection results in an increase of S100A9 expression in the Dorsal Root Ganglia (DRGs). Infiltrating neutrophils into the DRGs were the main source of S100A9 post HSV-1 infection. Functionally, genetic or pharmacological inhibition of S100A9 impairs the development of HSV-1 infection-induced mechanical pain hypersensitivity. Finally, we found that the pronociceptive role of S100A9 in herpetic neuralgia depends on the TLR4/TNF pathway. These results unraveled previously unknown mechanisms involved in the pathophysiology of herpetic neuralgia and indicate that S100A9 might be an important target for novel therapies aiming acute herpetic neuralgia. (AU) | |
| 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 |