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Objectives: The purpose of the present study was to investigate whether intramuscular BoNT/A injections cause an systemic inflammatory response and a local inflammatory response in the muscle tissue. Methods: Thirty-two male Sprague Dawley rats treated with BoNT/A (i.m., 1IU) were divided in four groups, depending on the time of BoNT/A injection (2 days before, 1, 2, and 4 weeks before the experiment). Bio-Plex Pro Rat Cytokine 23-plex Multiplex Assay (Bio-Rad, USA). Results: Systemic inflammation: 17 cytokines (IL1-α (p = 0.005), IL-1β (p = 0.01), IL-2 (p = 0.04), IL-4 (p = 0.03), IL-6 (p = 0.03), IL-10 (p = 0.02), IL12(p70) (p = 0.03), IL-13 (p = 0.04), IL-17 (p = 0.03), GM-CSF (p = 0.03), INF-γ (p = 0.03), MIP-1α (p = 0.03), MIP-3α (p = 0.04), RANTES (p = 0.001), TNF-α (p = 0.04), vascular endothelial growth factor (p = 0.03), and MCP-1 (p = 0.02)) showed significantly higher expression levels 2 days after intramuscular BoNT/A injections compared to other time points (1, 2, and 4 weeks). Local inflammation: 12 cytokines (IL-1β (p = 0.02), IL-6 (p = 0.002), IL-10 (p = 0.02), IL-13 (p = 0.04), IL-17 (p = 0.02), TNF-α (p = 0.001), GM-CSF (p = 0.01), M-CSF (p = 0.04), MIP-1α (p = 0.04), MIP-3α (p = 0.002), RANTES (p = 0.02), and MCP-1(p = 0.004)) showed higher expression levels 2 and/or 4 weeks after intramuscular BoNT/A injections compared to the other time points (2 days and 1 week). Conclusion: Intramuscular BoNT/A injections result in a rapid systemic inflammatory response that only lasts a couple of days. At the same time, intramuscular BoNT/A injections cause an inflammatory response locally in the muscle with significantly higher cytokine levels 2 and/or 4 weeks after injections. [ABSTRACT FROM AUTHOR]

Individuals with cerebral palsy (CP) develop skeletal muscle contractures that impair muscle function. In turn, contractures affect the ability to ambulate and often promote a sedentary lifestyle. The aim of the present study was to investigate the systemic inflammatory markers transforming growth factor beta-1 (TGFβ1), C-reactive protein (CRP), and interleukin-6 (IL-6) in children and adults with CP. Blood samples of n = 34 participants (24 individuals with CP (n = 14 children with CP age 10.36 ± 1.1 and n = 10 adults with CP age 38.80 ± 3.6) and 10 healthy adults age 36.63 ± 3.8) were analyzed for circulating levels of TGFβ1, CRP, and IL-6 using Sandwich Enzyme linked immunosorbent assay (ELISA) analyses (R&D systems). TGFβ1 and CRP levels were significantly higher in children with CP compared to both adults with CP (TGFβ1: P < 0.0005 and P < 0.0002, respectively) and healthy adults (CRP: P < 0.0001 and P < 0.0001, respectively), while no differences were observed between the adults with CP and healthy adults in TGFβ1 (P = 0.29) and CRP (P = 0.59), respectively. Furthermore, IL-6 levels showed no significant differences between the groups. The present findings indicate that the level of systemic inflammation is increased in children with CP. We speculate that persisting inflammation in children with CP might influence the development of muscle contractures, resulting in reduced muscle mass and marked muscle weakness in adults with CP. [ABSTRACT FROM AUTHOR]

Background: Achilles tendinopathy is a painful inflammatory condition characterized by swelling, stiffness and reduced function of the Achilles tendon. Kager’s fat pad is an adipose tissue located in the area anterior to the Achilles tendon. Observations reveal a close physical interplay between Kager’s fat pad and its surrounding structures during movement of the ankle, suggesting that Kager’s fat pad may stabilize and protect the mechanical function of the ankle joint. Aim: The aim of this study was to characterize whether Achilles tendinopathy was accompanied by changes in expression of inflammatory markers and metabolic enzymes in Kager’s fat pad. Methods: A biopsy was taken from Kager’s fat pad from 31 patients with chronic Achilles tendinopathy and from 13 healthy individuals. Gene expression was measured by reverse transcription-quantitative PCR. Focus was on genes related to inflammation and lipid metabolism. Results: Expression of the majority of analyzed inflammatory marker genes was increased in patients with Achilles tendinopathy compared to that in healthy controls. Expression patterns of the patient group were consistent with reduced lipolysis and increased fatty acid β-oxidation. In the fat pad, the pain-signaling neuropeptide substance P was found to be present in one third of the subjects in the Achilles tendinopathy group but in none of the healthy controls. Conclusion: Gene expression changes in Achilles tendinopathy patient samples were consistent with Kager’s fat pad being more inflamed than in the healthy control group. Additionally, the results indicate an altered lipid metabolism in Kager’s fat pad of Achilles tendinopathy patients. [ABSTRACT FROM AUTHOR]

Although histology data favour the view of a degenerative nature of tendinopathy, indirect support for inflammatory reactions to loading in affected tendons exists. The purpose of the present study was to elucidate whether inflammatory signalling responses after acute mechanical loading were more pronounced in tendinopathic versus healthy regions of human tendon and if treatment with non-steroidal anti-inflammatory medications (NSAID's) reduces this response. Twenty-seven tendinopathy patients (>6 months) were randomly assigned to a placebo ( n = 14) or NSAID (Ibumetin NYCOMED GmbH Plant Oranienburg Germany (600 mg) × 3/day/1 week) group ( n = 13) in a double-blinded-fashion. Tendon biopsies were taken from the painful and a healthy region of the same tendon 2 h after 1 h running. Gene-expression of several targets was analysed in the sampled Achilles tendon biopsies. The mRNA for TGF- $$\beta$$, collagen-I and collagen-III were significantly higher expressed, and decorin, CTGF, IL-6 and IL-10 were significantly lower expressed in the tendinopathic versus healthy tendon area. Only IL-10 was lower in expression in experiments with NSAID administration, while all other determined parameters were unaffected by NSAID. All ultrasonographic outcomes were unchanged in response to acute exercise and not influenced by NSAID. The signalling for collagen and TGF-beta was upregulated after acute loading in tendinopathic tendon. In contrast to the hypothesis, inflammatory signalling was not exaggerated in tendinopathic tendon 2 h after acute mechanical loading. [ABSTRACT FROM AUTHOR]