Abstract
ObjectiveThis 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.MethodsMale 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 h after CFA injection. von Frey test was used to assess mechanical hyperalgesia. Tissues from paw skin, paw 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. The macrophage phenotype at the inflammation site was evaluated by Western blotting assay using the Nitric Oxide Synthase 2 (NOS 2) and Arginase-1 immunocontent to identify M1 and M2 macrophages, respectively.ResultsOur results confirm a consistent analgesic effect of AJM following the second treatment session. AJM did not change cytokines levels at the inflammatory site, although it promoted a reduction in M2 macrophages. Also, there was a reduction in the levels of pro-inflammatory cytokines IL-1β and TNF in the spinal cord.ConclusionTaken 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.
Highlights
The inflammatory process is an essential mechanism of the immune system that allows the body to remove harmful stimuli and recover damaged tissue, restoring tissue homeostasis (Medzhitov, 2008; Ahmed, 2011)
Mechanical hyperalgesia was not reduced by the first ankle joint mobilization (AJM) treatment when comparing to the Complete Freund Adjuvant (CFA)/Sham and CFA/AJM groups
Mechanical hyperalgesia was observed for 24 h and in the subsequent periods evaluated in the CFA/Sham group when compared to the Saline/Sham group (p < 0.001)
Summary
The inflammatory process is an essential mechanism of the immune system that allows the body to remove harmful stimuli and recover damaged tissue, restoring tissue homeostasis (Medzhitov, 2008; Ahmed, 2011). The persistence of harmful stimulus and the impaired resolution of inflammation forms the basis of many chronic inflammatory diseases, including cardiovascular disease, diabetes, certain cancers and bowel, arthritis, and osteoporosis (Libby, 2007). In this way, inflammation is no longer a protective and specific response of the organism and can generate disorders such as chronic pain, sleep disorders, anxiety, and depression. This disease affects middleaged people, young people, and especially the elderly, causing pain and severe physical disability (Woolf and Pfleger, 2003; Smolen et al, 2016; Perretti et al, 2017)
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