Osteoarthritis (OA) is the leading degenerative joint disease in the western world and leads, if left untreated, to a progressive deterioration of joint functionality, ultimately reducing quality of life. Recent data has shown, that especially OA of the ankle and foot are among the most frequently affected regions. Current research in OA points towards a complex involvement of various cell and tissue types, often accompanied by inflammation. Low-dose radiotherapy (LDRT) is widely used for the treatment of degenerative and inflammatory diseases. While the reported analgesic effects are well known, the underlying molecular mechanisms are only poorly understood. We therefore correlated a clinical approach, looking at pain reduction in 196 patients treated with LDRT with a pre-clinical approach, utilizing the K/BxN serum transfer mouse model using flow cytometry and multiplex ELISA for analysis. While an improvement of symptoms in the majority of patients was found, patients suffering from symptoms within the tarsi transversa show a significantly lower level of improvement. Further, a significant impact of therapy success was detected depending on whether only one or both feet were affected. Further, patients of younger age showed a significantly better outcome than older ones while needing fewer treatment series. When looking on a cellular level within the mouse model, a systemic alteration of immune cells namely a shift from CD8+ to CD4+ T cells and reduced numbers of DCs was observed. A general reduction of inflammatory cytokines was detected, with significant alterations in IL-4 and IL-17 levels, all of which could potentially be responsible for the highly effective clinical improvement in patients. Taken together our data indicate that LDRT can be regarded as a highly effective treatment option for patients suffering from OA of the foot and ankle, in terms of analgesic effects, especially in younger patients. Furthermore, the observed effects are mediated by an interplay of cellular and soluble immune factors, as observed in the K/BxN serum transfer model. With this interdisciplinary approach we aim to encourage the usage of LDRT as an additive treatment strategy not only as a last resort, but also earlier in the course of disease.
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http://dx.doi.org/10.3389/fimmu.2021.777792 | DOI Listing |
Mol Med
December 2024
Key Laboratory of Viral Pathogenesis and Infection Prevention and Control (Jinan University), Ministry of Education, School of Medicine, Jinan University, Guangzhou, 510632, China.
Rheumatoid arthritis (RA) and cardiovascular disease (CVD) are both the chronic inflammatory disease. To investigate the influence of secondary atherosclerosis on arthritis mice, we treated the ApoE mice with K/BxN serum and high fat diet (HFD), and subsequently assessed the phenotypes as well as immune profiles of K/BxN serum and HFD induced ApoE mice. We found that HFD treatment aggravated the hyperlipidemia, atherosclerotic lesions, ankle swelling and arthropathy of mice.
View Article and Find Full Text PDFArthritis Res Ther
December 2024
Department of Medicine, University of California, 9500 Gilman Dr. MC 0663, La Jolla, San Diego, CA, USA.
Background: In the murine K/BxN serum transfer rheumatoid arthritis (RA) model, tactile allodynia persists after resolution of inflammation in male and partially in female wild type (WT) mice, which is absent in Toll-like receptor (TLR)4 deficient animals. We assessed the role of TLR4 on allodynia, bone remodeling and afferent sprouting in this model of arthritis.
Methods: K/BxN sera were injected into male and female mice with conditional or stable TLR4 deletion and controls.
Sci Transl Med
November 2024
Research Institute, Hospital for Special Surgery, New York, NY 10021, USA.
Macrophages are key drivers of inflammation and tissue damage in autoimmune diseases including rheumatoid arthritis. The rate-limiting step for transcription of more than 70% of inducible genes in macrophages is RNA polymerase II (Pol II) promoter-proximal pause release; however, the specific role of Pol II early elongation control in inflammation, and whether it can be modulated therapeutically, is unknown. Genetic ablation of a pause-stabilizing negative elongation factor (NELF) in macrophages did not affect baseline Pol II occupancy but enhanced the transcriptional response of paused anti-inflammatory genes to lipopolysaccharide followed by secondary attenuation of inflammatory signaling in vitro and in the K/BxN serum transfer mouse model of arthritis.
View Article and Find Full Text PDFSci Rep
November 2024
Department of Public Health and Pediatrics, University of Turin, Turin, Italy.
Eur J Pharmacol
December 2024
Inflammation and Immune Mediated Disease Laboratory of Anhui Province, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei, 230032, China. Electronic address:
Background: Rheumatoid arthritis (RA) is characterized by chronic inflammation of the synovium of joints. Fibroblast-like synoviocytes (FLS) play an important role in RA pathogenesis. We aimed to investigate the effect of N-(4-methoxyphenyl) quinoline-8-sulfonamide (QS-3g) on the inflammatory response of FLS and explore the potential underlying mechanisms.
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