Interferon- beta 1a administration results in a transient increase of serum amyloid A protein and C-reactive protein: comparison with other markers of inflammation

Putative markers of inflammation such as serum beta 2-microglobulin and neopterin have been shown to be transiently upregulated following interferon- beta (IFN- beta ) 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- beta 1a (Avonex). This pattern of expression was found to parallel that of beta 2-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- beta 1a 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- beta 1a injected on a weekly basis did not produce a sustained modulation of any of the markers investigated in patients treated for 32 weeks.