It is well established that arthritis depresses locomotion in humans as well as in animal disease models. The K/BxN mouse model resembles rheumatoid arthritis and is widely used for research. Here, we investigate the behavioral alterations of arthritic K/BxN mice during arthritis development with respect to horizontal locomotion. Locomotor activity measurements and the methodology of ankle thickness measurements are compared to demonstrate the feasibility of motion tracking in the K/BxN mouse model. Arthritic K/BxN mice show significantly decreased locomotion compared to their non-arthritis K/BxN littermates. We found an indirect correlation of ankle thickness and locomotor activity. However, both parameters are only partially interdependent resulting in temporal displacement of maximal ankle swelling and maximal depression of locomotion by 1 week. Assessing the impaired movement as a behavioral test appears to be a valuable multifactorial parameter for the evaluation of arthritis in the K/BxN mouse model and provides additional information on disease progression and severity.
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http://dx.doi.org/10.1007/s00296-011-2337-5 | 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 PDFArthritis Res Ther
November 2024
Department of Orthopaedic Surgery, Washington University in St. Louis, St. Louis, MO, 63110, USA.
Background: Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by increased levels of inflammation that primarily manifests in the joints. Macrophages act as key drivers for the progression of RA, contributing to the perpetuation of chronic inflammation and dysregulation of pro-inflammatory cytokines such as interleukin 1 (IL-1). The goal of this study was to develop a macrophage-based cell therapy for biologic drug delivery in an autoregulated manner.
View Article and Find Full Text PDFSci Rep
November 2024
Department of Public Health and Pediatrics, University of Turin, Turin, Italy.
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