Here we aimed to determine the therapeutic effect of allicin on ankylosing spondylitis (AS) and explore the mechanism(s) of action. AS mouse model was constructed by transferring the HLA-B2704 gene into Kunming mice and verified by RT-PCR and CT imaging. Verified AS mice were randomly divided into model group (n = 6) and allicin-treated groups (50, 100, and 200 mg/kg, resp., n = 6, p.o., for 2 months). Wild type mice were used as control (n = 6). The levels of AS-related inflammatory factors were measured by ELISA. mRNA and protein expressions of HLA-B27 were checked by RT-PCR and western blotting. As the results, the mouse model of AS was successfully established, and high-dose allicin could markedly alleviate spine inflammatory injury possibly via reducing the secretion of the inflammatory factors (IL-6, IL-8, and TNF- α ) sharply in AS mice. Moreover, allicin significantly inhibited HLA-B27 protein translation but failed to suppress HLA-B27 gene transcription in AS mice, indicating a posttranscriptional mechanism of this modulation. In conclusion, allicin has potential to be used for AS treatment as an anti-inflammatory nutraceutical.
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http://dx.doi.org/10.1155/2013/171573 | DOI Listing |
Curr Rheumatol Rep
December 2024
Department of Medicine, Division of Rheumatology, Queen's University, Kingston, ON, Canada.
Purpose Of Review: The canonical pathogenesis of spondyloarthritis (SpA) involves inflammation driven by HLA-B27, type 3 immunity, and gut microbial dysregulation. This review based on information presented at the SPARTAN meeting highlights studies on the pathogenesis of SpA from the past year, focusing on emerging mechanisms such as the roles of microbe-derived metabolites, microRNAs (miRNAs) and cytokines in plasma exosomes, specific T cell subsets, and neutrophils.
Recent Findings: The induction of arthritis in a preclinical model through microbiota-driven alterations in tryptophan catabolism provides new insights as to how intestinal dysbiosis may activate disease via the gut-joint axis.
Rheumatology (Oxford)
December 2024
Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds, UK.
Axial involvement in psoriatic arthritis (PsA) has been a major feature of the disease since the original description by Wright and Moll. However, despite over 50 years of study, there is still no accepted definition of axial PsA, nor validated classification criteria. Numerous observational studies have described a phenotype of axial involvement that differs from classical ankylosing spondylitis (AS or axial spondyloarthritis) both clinically and radiographically, and in the frequency of the HLA-B27 antigen.
View Article and Find Full Text PDFMetabolomics
December 2024
U1177 - Drugs and Molecules for living Systems, Univ. Lille, Inserm, Institut Pasteur de Lille, F-59000, Lille, France.
Introduction: Inflammatory bowel diseases (IBDs) are chronic immune driven intestinal disorders with marked metabolic alteration. Mass spectrometry imaging (MSI) enables the direct visualization of biomolecules within tissues and facilitates the study of metabolic changes. Integrating multiple spatial information sources is a promising approach for discovering new biomarkers and understanding biochemical alteration within the context of the disease.
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
State Key Laboratory of Pharmaceutical Biotechnology, Chemistry and Biomedicine Innovation Center (ChemBIC), School of Life Sciences, Nanjing University, 163 Xianlin Avenue, Nanjing 210023, Jiangsu, China. Electronic address:
Ankylosing spondylitis (AS) is an autoimmune rheumatic disease that primarily affects the axial joints, with its etiology complex and still not fully understood. The unknown pathogenesis of AS limits the development of treatment strategies, so keeping up-to-date with the current research on AS can help in searching for potential therapeutic targets. In addition to the classic HLA-B27 genetic susceptibility and Th17-related inflammatory signals, increasing research is focusing on the influence of autoantigen-centered autoimmune responses and bone stromal cells on the onset of AS.
View Article and Find Full Text PDFNat Rev Rheumatol
December 2024
Pediatric Translational Research Branch, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, USA.
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