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Interleukin-17A during local and systemic Staphylococcus aureus-induced arthritis in mice.

Journal article
Authors Louise Henningsson
Pernilla Jirholt
Catharina Lindholm
Tove Eneljung
Elin Silverpil
Yoichiro Iwakura
Anders Lindén
Inger Gjertsson
Published in Infection and immunity
Volume 78
Issue 9
Pages 3783-90
ISSN 1098-5522
Publication year 2010
Published at Institute of Medicine, Department of Rheumatology and Inflammation Research
Institute of Medicine
Pages 3783-90
Language en
Links dx.doi.org/10.1128/IAI.00385-10
Keywords Animals, Arthritis, Infectious, immunology, Female, Granulocyte Colony-Stimulating Factor, blood, Interferon-gamma, physiology, Interleukin-17, blood, physiology, Kidney, microbiology, Male, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Knockout, Neutrophils, immunology, Staphylococcal Infections, immunology, Staphylococcus aureus
Subject categories Infectious Medicine

Abstract

Staphylococcus aureus is one of the dominant pathogens that induce septic arthritis in immunocompromised hosts, e.g., patients suffering from rheumatoid arthritis treated with immunosuppressive drugs. S. aureus-induced arthritis leads to severe joint destruction and high mortality despite antibiotic treatment. Recently, interleukin-17A (IL-17A) has been discovered to be an important mediator of aseptic arthritis both in mice and humans, but its function in S. aureus-induced arthritis is largely unknown. Here, we investigated the role of IL-17A in host defense against arthritis following systemic and local S. aureus infection in vivo. IL-17A knockout mice and wild-type mice were inoculated systemically (intravenously) or locally (intra-articularly) with S. aureus. During systemic infection, IL-17A knockout mice lost significantly more weight than the wild-type mice did, but no differences were found in the mortality rate. The absence of IL-17A had no impact on clinical arthritis development but led to increased histopathological erosivity late during systemic S. aureus infection. Bacterial clearance in kidneys was increased in IL-17A knockout mice compared to the level in wild-type mice only 1 day after bacterial inoculation. During systemic S. aureus infection, serum IL-17F protein levels and mRNA levels in the lymph nodes were elevated in the IL-17A knockout mice compared to the level in wild-type mice. In contrast to systemic infection, the IL-17A knockout mice had increased synovitis and erosions and locally decreased clearance of bacteria 3 days after local bacterial inoculation. On the basis of these findings, we suggest that IL-17A is more important in local host defense than in systemic host defense against S. aureus-induced arthritis.

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