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Antibiotic-killed Staphylococcus aureus induces destructive arthritis in mice.

Journal article
Authors Abukar Ali
Xuefeng Zhu
Jakub Kwiecinski
Inger Gjertsson
Catharina Lindholm
Yoichiro Iwakura
Xiaoyang Wang
Nils Y Lycke
Elisabet Josefsson
Rille Pullerits
Tao Jin
Published in Arthritis & rheumatology (Hoboken, N.J.)
Volume 67
Issue 1
Pages 107-116
ISSN 2326-5205
Publication year 2015
Published at Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation
Institute of Medicine, Department of Rheumatology and Inflammation Research
Institute of Biomedicine, Department of Microbiology and Immunology
Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Pages 107-116
Language en
Links dx.doi.org/10.1002/art.38902
https://gup.ub.gu.se/file/148124
Keywords RAGE; Staphylococcus aureus; TLR2; TNF-α; antibiotics; arthritis
Subject categories Infectious Medicine, Rheumatology and Autoimmunity

Abstract

Objective: Permanent reduction in joint function is a severe post-infectious complication in patients with Staphylococcus aureus septic arthritis. This reduction in joint function might be caused by persistent joint inflammation after the adequate eradication of bacteria by antibiotics. Methods: We studied whether antibiotic-killed S. aureus induced joint inflammation in mice and elucidated the molecular and cellular mechanism of this type of arthritis. Results: The intraarticular injection of antibiotic-killed S. aureus induced mild to moderate synovitis and bone erosions that lasted for a minimum of 14 days. The frequency and severity of synovitis were significantly reduced in tumor necrosis factor receptor 1 (TNFR1), receptor for Advanced Glycation End Products (RAGE), and toll like receptor 2 (TLR2) knockout mice compared with wild-type animals. The combined depletion of monocytes and neutrophils resulted in a significantly lower frequency of synovitis. Among bacterial factors, insoluble cell debris played a more important role than bacterial DNA or soluble components in inducing joint inflammation. Importantly, anti-TNF therapy abrogated the joint inflammation induced by antibiotic-killed S. aureus. Conclusion: Antibiotic-killed S. aureus induced and maintained the joint inflammation that is mediated through TLR2, TNFR1, and RAGE receptor. The cross-talk between neutrophils and monocytes is responsible for this type of arthritis. Anti-TNF therapy might be used as a novel therapeutic strategy, in combination with antibiotics, to treat staphylococcal septic arthritis. © 2014 American College of Rheumatology.

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