Received for publication December 28, 2005.
Revised March 21, 2006.
Accepted for publication March 28, 2006.

Serum amyloid A induces contrary immune responses via formyl peptide receptor like-1 in human monocytes

Abstract

Although the level of serum amyloid A has been reported to be up-regulated during inflammatory response, the role of serum amyloid A on the regulation of inflammation and immune response has not been elucidated. We found that serum amyloid A stimulated the production of tumor necrosis factor- (TNF-) and IL-10, which are, proinflammatory and anti-inflammatory cytokines, respectively in human monocytes. Low concentrations of serum amyloid A stimulated TNF- production with maximal activity at 6 hr after stimulation, whereas high concentrations of serum amyloid A stimulated IL-10 production with maximal activity at 12 hr. The activations of the two cytokines by serum amyloid A occurred at both the transcription and translational levels. Signaling events induced by serum amyloid A included the activation of two mitogen activated protein kinase (extracellular signal-regulated kinase and p38 kinase), which were found to be required for TNF- and IL-10 production, respectively. The stimulation of formyl peptide receptor like 1-expressing RBL-2H3 cells, but not of vector-expressing RBL-2H3 cells with serum amyloid A, induced mitogen activated protein kinases activation and the accumulation of the RNAs of these two cytokines. Taken together, our findings suggest that serum amyloid A modulates contrary immune responses via formyl peptide receptor like 1, by inducing TNF- or IL-10, and demonstrate that extracellular signal-regulated kinase and p38 kinase play counteracting roles in this process.

Key words: Interleukins, Gi family, Calcium (G Protein Coupled Signals), MAP Kinase, P38 MAP Kinase

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