A novel function of serum amyloid A: a potent stimulus for the release of tumor necrosis factor-alpha, interleukin-1beta, and interleukin-8 by human blood neutrophil.
High density lipoprotein (HDL) and its main apolipoproteins, AI and serum amyloid A (SAA), present in physiological and acute phase response conditions, respectively, affect the inflammatory process. This study focuses on the effect of AI, SAA, and HDL from healthy (N-HDL) and acute phase individuals (AP-HDL) on the release of TNF-alpha, IL-1beta, and IL-8 by human blood neutrophils. It was observed that SAA (100 microg/mL) causes a dramatic increase (75-400 times) in the basal liberation of the three cytokines assayed. This effect is not triggered by AP-HDL. Although AI (100 microg/ml) increases the release of IL-1beta and IL-8 modestly, N-HDL does not. Both HDLs (0.16-0.32 mg of protein/mL) had an anti-inflammatory action, decreasing the basal and LPS-stimulated cytokine release. Given that the biological role of SAA is still uncertain, the present study adds an important finding potentially pertinent to the biological role of this acute phase protein.
Furlaneto
C J
CJ
Departamento de Análises Clínicas e Toxicológicas, Faculdade de Ciências Farmacêuticas, Universidade de São Paulo, São Paulo, CEP 05508-900, Brazil.
Campa
A
A
D016632:Apolipoprotein A-I / Q000378:metabolism; D002478:Cells, Cultured; D016207:Cytokines / Q000378:metabolism*; D006801:Humans; D007375:Interleukin-1 / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D008075:Lipoproteins, HDL / Q000378:metabolism; D009504:Neutrophils / Q000378:metabolism*; D000685:Serum Amyloid A Protein / Q000378:metabolism / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D016632:Apolipoprotein A-I; D016207:Cytokines; D007375:Interleukin-1; D016209:Interleukin-8; D008075:Lipoproteins, HDL; D000685:Serum Amyloid A Protein; D014409:Tumor Necrosis Factor-alpha