Mobilização articular de tornozelo promove efeito neuroimunomodulatório em modelo de dor inflamatória em camundongos

• Ano de defesa: 2020
• Autor(a) principal: Omura, Carlos Minoru
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Palavras-chave em Português: Mobilização articular; Terapia Manual; Neuroimunomodulação; Citocinas inflamatórias; Macrófagos
• Link de acesso: https://repositorio.animaeducacao.com.br/handle/ANIMA/15154

Introduction: This study aims to investigate the effects of ankle joint mobilization (AJM) on mechanical hyperalgesia and peripheral and central inflammatory biomarkers after intraplantar (i.pl.) Complete Freund's Adjuvant (CFA)-induced inflammation. Methodology: Male Swiss mice were randomly assigned to 3 groups (n = 7): Saline/Sham, CFA/Sham, and CFA/AJM. Five AJM sessions were carried out at 6, 24, 48, 72, and 96 hours after the model induction. The von Frey test was used to assess mechanical hyperalgesia. To investigate the immunomodulatory mechanisms at the inflammation site and the central modulation underlying the analgesic effects of AJM, the paw skin and muscle and spinal cord were collected to measure pro-inflammatory (TNF, IL-1β) and anti-inflammatory cytokines (IL-4, IL-10, and TGF-β1) by ELISA 98 hours after CFA injection. The macrophage phenotype at the inflammation site was evaluated using the NOS 2 (M1) and Arginase-1 (M2) immunocontent in the Western blotting assay. Results: Our results confirm a consistent analgesic effect of AJM following the second treatment. AJM did not change cytokines levels at the inflammation site, although it promoted a reduction in M2 macrophages. However, there was a reduction in the levels of pro-inflammatory cytokines IL-1β and TNF in the spinal cord. Taken together, the results confirm the anti-hyperalgesic effect of AJM and suggest a central neuroimmunomodulatory effect in a model of persistent inflammation targeting the pro-inflammatory cytokines IL-1β and TNF. Conclusion: These findings support that AJM can improve pain-induced inflammatory pathologies and modify the underlying pathological process.