Serum amyloid A transcription in Atlantic salmon (Salmo salar L.) hepatocytes is enhanced by stimulation with macrophage factors, recombinant human IL-1 beta, IL-6 and TNF alpha or bacterial lipopolysaccharide
Jb. Jorgensen et al., Serum amyloid A transcription in Atlantic salmon (Salmo salar L.) hepatocytes is enhanced by stimulation with macrophage factors, recombinant human IL-1 beta, IL-6 and TNF alpha or bacterial lipopolysaccharide, DEV COMP IM, 24(6-7), 2000, pp. 553-563
Serum amyloid A (B-SAA) has previously been reported to be an acute-phase p
rotein in salmonids. Hepatocytes represent a major source of A-SAA in salmo
nids, but nothing is known about hepatocyte SAA synthesis in fish. In the p
resent work, the expression of A-SAA transcripts in primary cultures of Atl
antic salmon hepatocytes in response to macrophage derived cytokines, human
recombinant cytokines and bacterial lipopolysaccharide (LPS) was studied b
y Northern blot analysis. The macrophage supernatants were prepared by stim
ulating Atlantic salmon head kidney macrophages with LPS, yeast glucan or a
leukocyte derived macrophage activating factor (MAF). The supernatants fro
m glucan- or MAF-stimulated macrophages had no effect on A-SAA expression o
f the hepatocytes while supernatants from LPS-stimulated macrophages gave a
bout a 2-fold increase in expression. The combination of either glucan and
MAF, or LPS and MAF were more effective and these supernatants gave a 3.4-
and 5.2-fold increase in A-SAA expression, respectively. The hepatocytes we
re also treated with the human recombinant cytokines TNF alpha, IL-1 beta a
nd IL-6, alone or in combination. The A-SAA response to each of them alone
was modest, but TNF alpha and IL-6 or IL-1 beta and IL-6 in combination gav
e a higher response than each cytokine alone. These data suggest that the e
xpression of A-SAA by hepatocytes from Atlantic salmon is induced by cytoki
ne-like molecules. Interestingly, hepatocytes treated directly with LPS gav
e a more than 10-fold increase in SAA mRNA expression, but it is not known
if this is a direct effect of LPS on the hepatocytes or if it is mediated b
y other contaminating cell types. (C) 2000 Elsevier Science Ltd. All rights
reserved.