Role of afferent nociceptive fibers on the anti-hyperalgesic acupuncture effect in...
| Full text | |
| Author(s): Show less - |
Lopes, Alexandre H.
[1]
;
Talbot, Jhimmy
[1]
;
Silva, Rangel L.
[1]
;
Lima, Jonilson B.
[1]
;
Franca, Rafael O.
[1]
;
Verri, Jr., Waldiceu A.
[2]
;
Mascarenhas, Danielle P.
[3]
;
Ryffel, Bernhard
[4, 5]
;
Cunha, Fernando Q.
[1, 3]
;
Zamboni, Dario S.
;
Cunha, Thiago M.
[1]
Total Authors: 11
|
| Affiliation: | [1] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Pharmacol, BR-14049900 Sao Paulo - Brazil
[2] Univ Estadual Londrina, Ctr Ciencias Biol, Dept Ciencias Patol, Londnna, Parana - Brazil
[3] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Cell Biol, BR-14049900 Sao Paulo - Brazil
[4] Univ Orleans, Orleans - France
[5] CNRS, UMR7355, Expt & Mol Immunol & Neurogenet, F-45071 Orleans - France
Total Affiliations: 5
|
| Document type: | Journal article |
| Source: | Pain; v. 156, n. 3, p. 451-459, MAR 2015. |
| Web of Science Citations: | 10 |
| Abstract | |
Inflammatory hyperalgesia is a complex process that depends on the sensitization of primary nociceptive neuron S triggered by proinflammatory mediators, such as interleukin 1 beta (IL-1 beta). Recently, the peripheral activation of caspase-1 (previously known as IL1-beta-converting enzyme) was implicated in the induction of acute inflammatory pain by promoting the processing of IL-1 beta from its precursor form, pro-IL-1 beta. Caspase-1 activation in several systems requires the assembly of an intracellular molecular platform called an inflammasome. Inflammasomes consist of 1 nucleotide-binding oligomerization domain-like receptor (NLR), the adapter molecule apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain (ASC), and caspase-1. NLRP3 and NLRC4 inflammasomes are well described. However, the identity of the inflamniasome that is-involved in the peripheral activation of caspase-1 that accounts for acute inflammatory hyperalgesia has not been described. The present findings demonstrated that mice deficient in NLRC4 or ASC, but not in NLRP3, present reduced mechanical and thermal acute inflammatory hyperalgesia induced by carrageenan. The reduced hyperalgesia was accompanied by significant impairments in the levels of mature forms of IL-1 beta (p17) and caspase-1 (p20) compared to wild-type mice at the inflammatory site. Therefore, these results identified the inflammasome components NLRC4 and ASC as the molecular platform involved in the peripheral activation of caspase-1 and IL-1 beta maturation, which are responsible for the induction of acute inflammatory pain. In conclusion, our study -provides new therapeutic targets for the control of acute inflammatory pain. (AU) | |
| FAPESP's process: | 13/08216-2 - CRID - Center for Research in Inflammatory Diseases |
| Grantee: | Fernando de Queiroz Cunha |
| Support type: | 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 type: | Research Projects - Thematic Grants |