Tumor necrosis factor alpha and prostaglandin E2 production by human monocyte-derived macrophages infected with spotted fever group rickettsiae

• Published in: Annals of the New York Academy of Sciences Vol. 590; p. 157
• Main Authors: Manor, E, Sarov, I
• Format: Journal Article
• Language: English
• Published: United States 01.01.1990
• Subjects: Dexamethasone - pharmacology; Dinoprostone - biosynthesis; Humans; Macrophages - metabolism; Macrophages - microbiology; Monocytes - metabolism; Rickettsia Infections - metabolism; Tumor Necrosis Factor-alpha - biosynthesis
• ISSN: 0077-8923
• DOI: 10.1111/j.1749-6632.1990.tb42218.x

Infection of macrophages by intracellular parasites might modulate production of tumor necrosis factor (TNF) and prostaglandin E2 (PGE2), which, in turn, might have a profound effect on the outcome of the infection in vivo. In this study we examined in an in vitro system, the rickettsial yield in human monocyte-derived macrophages (MdM) and the PGE2 and TNF production by MdM infected with Rickettsia conorii RC, Casablanca strain) or Israeli spotted fever (ISF, G-212 strain). TNF and PGE2 were determined in the media of MdM infected with RC or ISF. TNF reached maximum levels 24 h post-infection and then declined, while PGE2 levels increased continuously during the infection up to 96 h post-infection. Addition of dexamethasone inhibited both TNF and PGE2 production and enhanced rickettsial yield in MdM. Inhibition of PGE2 production by indomethacin resulted in increased production of TNF from rickettsial-infected MdM, while addition of PGE2 caused partial inhibition of TNF production from infected MdM.