Prostaglandin E2 inhibits the release of tumor necrosis factor-α, rather than interleukin 1β, from human macrophages
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Cited by (52)
Direct and indirect modulation of LPS-induced cytokine production by insulin in human macrophages
2020, CytokineCitation Excerpt :The impact of PGE2 on the progression of inflammation is ambivalent as it may inhibit or enhance the production of different cytokines via the same set of receptors in macrophages [31]. PGE2 clearly inhibited the stimulus-dependent expression and secretion of TNFα in Kupffer cells and other macrophages [32–35,31]. However, in one study [36] PGE2 increased TNFα formation at low concentrations and an inhibition of TNFα formation was only observed at high concentrations of PGE2.
Fever and sickness behavior: Friend or foe?
2015, Brain, Behavior, and ImmunityBacterial endotoxin induced hypothermia in pregnant rats: Role of tumor necrosis factor-α
2010, Journal of Thermal BiologyCitation Excerpt :With regard to potential mechanisms, Kozak et al. (1994, 1997) have reported that indomethacin potentiates plasma TNF-α activity and accentuates the transient decrease in core temperature that occurs in mice following ip administration of a relatively large dose of LPS. These data are in keeping with earlier reports that ibuprofen enhanced the release of TNF-α into the circulation of humans given LPS (Martich et al., 1991) and that prostaglandins – especially PGE2 – exert a negative feedback on in vitro TNF-α production (Kunkel et al., 1986; Fieren et al., 1991). Perhaps an attenuated PGE2 response secondary to a significantly reduced LPS-induced cyclooxygenase-2 activity during pregnancy plays a role in mediating the aforementioned accentuated TNF-α response (Fewell et al., 2002; Mouihate et al., 2002; Imai-Matsumura et al., 2002); this is currently being investigated in our laboratory.
Studies on the role of acid sphingomyelinase and ceramide in the regulation of tumor necrosis factor α (TNFα)-converting enzyme activity and TNFα secretion in macrophages
2010, Journal of Biological ChemistryCitation Excerpt :No statistically significant differences were detected in respect to the levels of IL-1β or prostaglandin E2 (data not shown). Because the latter is a negative regulator of TNFα secretion (48–50), these results suggest that the differences in TNFα secretion cannot be explained by differences in prostaglandin E2 production. Similarly, the simultaneous treatment with IL-6, which also can suppress TNFα synthesis, had no effect on the genotype-related differences (data not shown).
Activation of cytosolic phospholipase A<inf>2</inf>α in resident peritoneal macrophages by Listeria monocytogenes involves listeriolysin O and TLR2
2008, Journal of Biological ChemistryCitation Excerpt :The ability of indomethacin to enhance production of TNFα in cPLA2α+/+ macrophages to the level produced by cPLA2α-/- macrophages in response to L. monocytogenes suggests that prostaglandins act in an autocrine fashion to suppress TNFα production. It has been reported that TNFα production by human and mouse macrophages, including Kupffer cells, is suppressed by exogenous addition of prostaglandins and enhanced by blocking endogenous prostaglandin production with cyclooxygenase inhibitors (35-43). We show that this regulatory program is initiated by the activation of cPLA2α in response to L. monocytogenes infection.
Cyclooxygenase inhibition in human monocytes increases endotoxin-induced TNFα without affecting cyclooxygenase-2 expression
2004, European Journal of PharmacologyCitation Excerpt :The absence of detectable effects of cyclooxygenase inhibitors in spite of clear TNFα inhibition by exogenous prostaglandin E2 has led to the suggestion that thromboxane A2 counteracts the inhibitory effect of prostaglandin E2; thus cyclooxygenase inhibition would suppress in parallel the biosynthesis of stimulatory (thromboxane A2) and inhibitory (prostaglandin E2) factors explaining the absence of a detectable net effect on TNFα expression (Caughey et al., 1997). The studies mentioned above seem in contrast to a number of other studies (e.g., Endres et al., 1996; Fieren et al., 1992; Hart et al., 1989; Spatafora et al., 1991), which have employed cyclooxygenase inhibitors to block endogenous prostaglandin biosynthesis and find clear stimulation of TNFα. Thus, a nearly 6-fold increase of endotoxin-stimulated TNFα formation by 10 μM indomethacin has been reported in a macrophage cell line (Ikegami et al., 2001).
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On leave from the Department of Human Microbiology, Sackler School of Medicine, Tel Aviv University, Tel-Aviv, Israel.