Macrophage-mediated tumor cell killing: lack of dependence on the cyclooxygenase pathway of prostaglandin synthesis.

Abstract

M phi obtained directly from disaggregated murine Moloney sarcomas produced PGE2 and a hydroxy fatty acid derivative as the major products of arachidonic acid metabolism. M phi-immunoreactive PGE synthetic rates decreased substantially and cytotoxic activity was lost when freshly explanted tumor M phi were held in culture 24 hr. Such cultured M phi remained in a partially activated "primed" state, however, wherein the addition of minute (ng) amounts of bacterial lipopolysaccharide (LPS) returned cytolytic activity and PGE synthesis to original levels. Indomethacin-induced blockade of the M phi cyclooxygenase pathway inhibited PG synthesis by LPS-stimulated, primed M phi without affecting the return of cytolytic activity. We conclude, therefore, that the production of PG had no direct role in the mediation of tumor cell killing by activated M phi isolated from these neoplasms.

• Authors: J O Shaw, S W Russell, M P Printz, R A Skidgel
• Journal: Journal of immunology (Baltimore, Md. : 1950) (J Immunol) Vol. 123 Issue 1 Pg. 50-4 (Jul 1979) ISSN: 0022-1767 [Print] United States
• PMID: 109539 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Arachidonic Acids
• Prostaglandins
• Prostaglandin-Endoperoxide Synthases

Topics

• Animals
• Arachidonic Acids (metabolism)
• Cytotoxicity, Immunologic
• Leukemia, Experimental (immunology)
• Macrophages (immunology)
• Mice
• Moloney murine leukemia virus (immunology)
• Prostaglandin-Endoperoxide Synthases (metabolism)
• Prostaglandins (biosynthesis)