Response to mechanical loading in rat Achilles tendon healing is influenced by the microbiome.

PLoS One

Orthopedics, Department of Biomedical and Clinical Sciences, Division of Surgery, Orthopedics and Oncology, Faculty of Medicine and Health Science, Linköping University, Linköping, Sweden.

Published: June 2020

We have previously shown that changes in the microbiome influence how the healing tendon responds to different treatments. The aim of this study was to investigate if changes in the microbiome influence the response to mechanical loading during tendon healing. 90 Sprague-Dawley rats were used. Specific Opportunist and Pathogen Free (SOPF) rats were co-housed with Specific Pathogen Free (SPF) rats, carrying Staphylococcus aureus and other opportunistic microbes. After 6 weeks of co-housing, the SOPF rats were contaminated which was confirmed by Staphylococcus aureus growth. Clean SOPF rats were used as controls. The rats were randomized to full loading or partial unloading by Botox injections in their calf muscles followed by complete Achilles tendon transection. Eight days later, the healing tendons were tested mechanically. The results were analysed by a 2-way ANOVA with interaction between loading and contamination on peak force as the primary outcome and there was an interaction for both peak force (p = 0.049) and stiffness (p = 0.033). Furthermore, partial unloading had a profound effect on most outcome variables. In conclusion, the response to mechanical loading during tendon healing is influenced by changes in the microbiome. Studies aiming for clinical relevance should therefore consider the microbiome of laboratory animals.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7064237PMC
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0229908PLOS

Publication Analysis

Top Keywords

response mechanical
12
mechanical loading
12
tendon healing
12
changes microbiome
12
sopf rats
12
achilles tendon
8
healing influenced
8
microbiome influence
8
loading tendon
8
pathogen free
8

Similar Publications

Bacterial Nanovesicles as Interkingdom Signaling Moieties Mediating Pain Hypersensitivity.

ACS Nano

January 2025

Department of Internal Medicine-Gerontology and Geriatric Medicine, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157, United States.

Gut dysbiosis contributes to multiple pathologies, yet the mechanisms of the gut microbiota-mediated influence on systemic and distant responses remain largely elusive. This study aimed to identify the role of nanosized bacterial extracellular vesicles (bEVs) in mediating allodynia, i.e.

View Article and Find Full Text PDF

Resonance-Induced Therapeutic Technique for Skin Cancer Cells.

Ultrasound Med Biol

January 2025

Institute of Biomedical Technologies, Auckland University of Technology, Auckland City, 1010, Auckland, New Zealand. Electronic address:

Objective: This study aims to evaluate the viability of a hypothesis for selective targeting of skin cancer cells by exploiting the spectral gap with healthy cells using analytical and numerical simulation.

Methods: The spectral gap was first identified using a viscoelastic dynamic model, with the physical and mechanical properties of healthy and cancerous skin cells deduced from previous experimental studies conducted on cell lines. The outcome of the analytical simulation was verified numerically using modal and harmonic analysis.

View Article and Find Full Text PDF

Endothelial cell (EC)-specific CTGF/CCN2 Expression Increases EC Reprogramming and Atherosclerosis.

Matrix Biol

January 2025

Department of Surgery, Emory University, Atlanta, GA, USA; Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA; Research Services, Atlanta VA Medical Center, Decatur, GA, USA. Electronic address:

Arterial endothelial cells (ECs) reside in a complex biomechanical environment. ECs sense and respond to wall shear stress. Low and oscillatory wall shear stress is characteristic of disturbed flow and commonly found at arterial bifurcations and around atherosclerotic plaques.

View Article and Find Full Text PDF

Dual effect of targeting LSD1 on the invasiveness and the mechanical response of acute lymphoblastic leukemia cells.

Biomed Pharmacother

January 2025

Department of Molecular Medicine, Centro de Investigaciones Biológicas Margarita Salas (CIB Margarita Salas-CSIC), Madrid, Spain. Electronic address:

Epigenetic alterations are hallmarks of cancer, with histone modifiers playing critical roles in gene transcription, DNA homeostasis, and other nuclear functions. Lysine-specific demethylase 1 (LSD1), a key regulator of H3K4 methylation, has emerged as a promising pharmacological target in cancer treatment, including leukemia. Acute lymphoblastic leukemia (ALL), the most common pediatric cancer, remains a significant therapeutic challenge due to limited understanding of how epigenetic therapy impacts leukemia dissemination.

View Article and Find Full Text PDF

Histamine H receptor blockade alleviates neuropathic pain through the regulation of glial cells activation.

Biomed Pharmacother

January 2025

Maj Institute of Pharmacology, Polish Academy of Sciences, Department of Neurochemistry, 12 Smetna Str., Krakow 31-343, Poland. Electronic address:

Neuropathic pain is a disorder affecting the somatosensory nervous system. However, this condition is also characterized by significant neuroinflammation, primarily involving CNS-resident non-neuronal cells. A promising target for developing new analgesics is histamine H receptor (HR); thus, we aimed to determine the influence of a novel HR antagonist/inverse agonist, E-98 (1-(7-(4-chlorophenoxy)heptyl)-3-methylpiperidine), on pain symptoms and glia activation in model of neuropathic pain in male mice (chronic constriction injury to the sciatic nerve).

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!