Platelet activating factor (PAF) can modulate macrophage responses such as mmoricidal and inflammatory activity induced by interferon gamma (IFNγ) or lipopolysaccharide (LPS). To determine how macrophage responsiveness to PAF was altered by IFNγ or LPS, PAF receptor-associated activities were studied. Pre-incubation of murine peritoneal macrophages with either LPS or IFNγ suppressed macrophage responsiveness to PAF-induced calcium mobilization and Superoxide anion production. This suppression of macrophage responsiveness to PAF was maximal following a 6 h preincubation with 25 u/ml EFNγ and 100 ng/ml LPS. Macrophages pre-treated with LPS alone or with IFNγ remained refractory to a PAF-induced rise in intracellular calcium for 24 h. In contrast, macrophages pre-incubated with 25 u/ml IFNγ alone remained refractory to PAF-induced calcium mobilization for 4 h. The suppression of PAF-induced calcium mobilization by LPS and IFNγ also decreased calcium-dependent O2 - production. In addition, treatment with LPS and IFNγ reduced specific [3H]PAF binding. Scatchard analysis demonstrated specific PAF binding sites on macrophages with two affinities. Incubation of macrophages with either LPS or IFNγ added alone or together led to a decrease in the number of cell surface PAF receptors and their binding affinity. These studies demonstrate that IFNγ and LPS can suppress select PAF-induced activities of macrophages. This suppression of PAF receptor activity may represent a means by which macrophages regulate the magnitude of a given response induced by PAF.
|Original language||English (US)|
|State||Published - 1996|
ASJC Scopus subject areas
- Agricultural and Biological Sciences (miscellaneous)
- Biochemistry, Genetics and Molecular Biology(all)
- Cell Biology