Reversal of ongoing proteinuria in autoimmune mice by treatment with C-reactive protein.

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  • Additional Information
    • Source:
      Publisher: Wiley-Blackwell Country of Publication: United States NLM ID: 0370605 Publication Model: Print Cited Medium: Print ISSN: 0004-3591 (Print) Linking ISSN: 00043591 NLM ISO Abbreviation: Arthritis Rheum Subsets: MEDLINE
    • Publication Information:
      Publication: : Hoboken, N.J. : Wiley-Blackwell
      Original Publication: Atlanta [etc.] Arthritis Foundation [etc.]
    • Subject Terms:
      Autoimmune Diseases/*drug therapy ; C-Reactive Protein/*therapeutic use ; Proteinuria/*drug therapy; Animals ; Autoantibodies/blood ; DNA/immunology ; Female ; Immunization ; Immunoglobulin G/immunology ; Interleukin-10/physiology ; Kidney Glomerulus/pathology ; Mice ; Mice, Inbred C57BL ; Mice, Inbred NZB
    • Abstract:
      Objective: To examine the ability of injection of C-reactive protein (CRP) to treat systemic lupus erythematosus (SLE) in the (NZB x NZW)F(1) (NZB/NZW) mouse and to use a nephrotoxic nephritis (NTN) model to further examine the mechanism of this activity.
      Methods: NZB/NZW mice were given a single injection of 200 mug of CRP prior to disease onset or after the onset of high-grade proteinuria. Mice were monitored weekly for proteinuria and monthly for anti-double-stranded DNA (anti-dsDNA) antibodies. NTN was induced by immunization with rabbit IgG followed by rabbit anti-mouse glomerular basement membrane. Proteinuria was measured daily, and renal pathology was scored. CRP was injected at the time of disease induction or 9 days later.
      Results: Treatment of NZB/NZW mice with CRP prior to disease onset delayed the onset of high-grade proteinuria by 16 weeks (P < 0.0001) and prolonged survival by 13 weeks (P < 0.002). CRP treatment of NZB/NZW mice during acute disease rapidly decreased proteinuria, and the treated mice remained aproteinuric for at least 10 weeks. Control and CRP-treated mice developed similar levels of anti-dsDNA. In C57BL/6 mice, injection of CRP either before or after induction of NTN suppressed proteinuria and glomerular pathology. CRP was completely ineffective in treating NTN in interleukin-10 (IL-10)-deficient mice.
      Conclusion: CRP injection suppresses inflammation in the kidney in SLE and NTN. The requirement for IL-10 in this protection suggests that CRP must rapidly initiate an IL-10-dependent antiinflammatory process. These findings suggest that a major function of CRP during the acute-phase response is to limit tissue damage and modulate acute inflammation.
    • Comments:
      Comment in: Arthritis Rheum. 2005 Feb;52(2):378-81. (PMID: 15692995)
    • Grant Information:
      AI-28358 United States AI NIAID NIH HHS
    • Accession Number:
      0 (Autoantibodies)
      0 (Immunoglobulin G)
      130068-27-8 (Interleukin-10)
      9007-41-4 (C-Reactive Protein)
      9007-49-2 (DNA)
    • Publication Date:
      Date Created: 20050205 Date Completed: 20050314 Latest Revision: 20220408
    • Publication Date:
      20231215
    • Accession Number:
      10.1002/art.20846
    • Accession Number:
      15692982