This study has evaluated the relationship between
tumor growth and induction of
acute-phase proteins. It has also determined whether an intact cellular immunity is obligatory for a fully expressed acute-phase
plasma protein response in the presence of a highly antigenic
tumor. Quantitatively,
acute-phase responses (
protein synthesis, plasma concentrations, hepatic
RNA content,
anorexia) were proportional to
tumor burden. Anti-inflammatory drugs (
indomethacin 1 micrograms/g body wt,
dexamethasone 0.5 micrograms/g body wt) had no direct effect on the attenuation of the systemic
acute-phase responses, but did affect them indirectly by decreasing
tumor growth. Immune suppression (
cyclosporine A at 20 or 60 micrograms/g body wt) had no effect on either acute-phase reactions or local
tumor growth. In
endotoxin-stimulated (
lipopolysaccharide) normal mice, immune suppression aggravated
anorexia and caused high mortality, while
dexamethasone partly reversed these effects in
endotoxin-stimulated mice. Plasma levels of
acute-phase proteins correlated to circulating levels of
IL-6 in untreated
tumor-bearing mice, but this relationship was not obvious in either
drug-treated
tumor-bearing or
endotoxin-stimulated mice.
Tumor tissue induced the synthesis of different
acute-phase proteins compared to
endotoxin. However, disintegrated normal liver tissue induced the synthesis of serum
amyloid protein to the same extent as the growing
tumor. This effect was primarily associated with the mitochondrial/lysosomal and microsomal liver cell fractions. In conclusion, the overall
acute-phase protein response is not a modulating factor of
tumor growth.(ABSTRACT TRUNCATED AT 250 WORDS)