Tumor necrosis factor alpha and prostaglandin E2 production by human monocyte-derived macrophages infected with spotted fever group rickettsiae.
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.
Manor
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Virology Unit, Faculty of Health Sciences, Ben Gurion University of the Negev, Beer Sheva, Israel.
Sarov
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I
D003907:Dexamethasone / Q000494:pharmacology; D015232:Dinoprostone / Q000096:biosynthesis*; D006801:Humans; D008264:Macrophages / Q000378:metabolism* / Q000382:microbiology; D009000:Monocytes / Q000378:metabolism; D012282:Rickettsia Infections / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis*
D014409:Tumor Necrosis Factor-alpha; D003907:Dexamethasone; D015232:Dinoprostone