Interferon-β1a administration results in a transient increase of serum amyloid A protein and C-reactive protein: comparison with other markers of inflammation

• Published in: Immunology letters 2001, Vol.75 (3), p.191-197
• Main Authors: Boylan, Michael T., Crockard, Alistair D., Duddy, Martin E., Armstrong, Marilyn A., McMillan, Stanley A., Hawkins, Stanley A.
• Format: Article
• Language: English
• Subjects: C-Reactive protein; Interferon-beta; Mononuclear leukocytes; Multiple sclerosis; Serum amyloid A protein
• ISSN: 0165-2478; 1879-0542
• DOI: 10.1016/S0165-2478(00)00310-2

Putative markers of inflammation such as serum β2-microglobulin and neopterin have been shown to be transiently upregulated following interferon-β (IFN-β) administration to multiple sclerosis (MS) patients. However, to date the role of the important inflammatory mediators serum amyloid A protein (SAA) and C-reactive protein (CRP) have not been described. Here we show that SAA but not CRP is elevated in relapsing-remitting MS patients compared to normal healthy individuals, and furthermore that both are transiently upregulated following intramuscular injection with IFN-β1a (Avonex™). This pattern of expression was found to parallel that of β2-microglobulin and neopterin following injection and was mirrored by a selective activation of peripheral monocytes with respect to upregulation of receptors known to be involved in the inflammatory response (HLA-DR, CD16 and CD86). Injection of saline solution intramuscularly to six healthy control individuals did not produce a similar upregulation of any of the inflammatory markers investigated. Following IFN-β1a injection, all inflammatory responses were attenuated at week 12 of therapy in comparison to those following the initial injection in a group of follow-up patients. In addition, IFN-β1a injected on a weekly basis did not produce a sustained modulation of any of the markers investigated in patients treated for 32 weeks.