Abstract
Peritoneal macrophages from amyloid resistant A/J mice produced more prostacyclin (PGI2) and protaglandin E (PGE2) and less thromboxane A2 (TXA2) into the incubation medium than similarly prepared macrophages from CBA/J mice. When CBA/J mice were given injections of azocasein sufficient to produce amyloid in the spleen, the amount of PGI2, but not PGE2 or TXA2 found in the medium from incubated macrophages was significantly decreased. This inhibition of PGI2 synthetase (and/or augmentation of PGI2 catabolism) was also found in the macrophages from azocasein treated A/J mice and to a lesser extent in water injected CBA/J and A/J mice. However, this inhibition of PGI2 synthetase in response to azocasein injections occurred much more slowly in the A/J macrophages than in the CBA/J macrophage. It is suggested that in the presence of elevated serum AA an altered arachidonic acid metabolism by cells of the mononuclear phagocytitic system may contribute to a susceptibility to amyloidosis.
This work was supported by the Veterans Administration and US PHS Grant #AM 32588.
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© 1986 Plenum Press, New York
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Leslie, C.A., Lazzarri, A., Cathcart, E.S. (1986). Prostacyclin and Thromboxane Production from Macrophages of Amyloid Resistant and Sensitive Mice. In: Glenner, G.G., Osserman, E.F., Benditt, E.P., Calkins, E., Cohen, A.S., Zucker-Franklin, D. (eds) Amyloidosis. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2199-6_21
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