Interaction with Complement Receptor 1 (CD35) Leads to Amelioration of Sepsis‐Triggered Mortality but Aggravation of Arthritis During Staphylococcus aureus Infection

The aim of this study was to assess the importance of complement receptor 1 (CR1, CD35) in Staphylococcus aureus arthritis and sepsis. The murine model of haematogenously acquired septic arthritis was used, injecting toxic shock syndrome toxin 1 (TSST‐1)‐producing S. aureus LS‐1 intravenously. CR1 w...

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Bibliographic Details
Published in:Scandinavian journal of immunology 1999-09, Vol.50 (3), p.250-255
Main Authors: Sakiniene, E, Heyman, B, Tarkowski, A
Format: Article
Language:English
Subjects:
Animals
Arthritis, Infectious - immunology
Arthritis, Infectious - microbiology
Arthritis, Infectious - physiopathology
Disease Models, Animal
Follow-Up Studies
Granulocytes - immunology
Leukocytes - immunology
Male
Mice
Phagocytosis - immunology
Rats
Receptors, Complement 3b - immunology
Sepsis - immunology
Sepsis - microbiology
Sepsis - mortality
Staphylococcal Infections - immunology
Staphylococcal Infections - microbiology
Staphylococcal Infections - mortality
Staphylococcal Infections - physiopathology
Staphylococcus aureus
T-Lymphocytes - immunology
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Summary:The aim of this study was to assess the importance of complement receptor 1 (CR1, CD35) in Staphylococcus aureus arthritis and sepsis. The murine model of haematogenously acquired septic arthritis was used, injecting toxic shock syndrome toxin 1 (TSST‐1)‐producing S. aureus LS‐1 intravenously. CR1 was blocked using immunoglobulin G (IgG) rat antimouse CR1 monoclonal antibody (MoAb) (8C12). Evaluation of arthritis was performed clinically and histopathologically. In addition, the effect of blocking CR1 was assessed on the phagocytic activity of leucocytes and on T‐cell dependent and independent inflammation. Seven days after inoculation with bacteria, 96% of CR1 MoAb‐treated mice had clinical symptoms of arthritis compared with 58% of the control animals (P 
ISSN:0300-9475
1365-3083
DOI:10.1046/j.1365-3083.1999.00595.x