Plasma levels of 15-keto-13,14-dihydro-prostaglandin E2 in patients with bronchogenic carcinoma

Starczewski, Michał; Voigtmann, R.; Peskar, Bernhard A.; Peskar, B. M.

doi:10.1016/0262-1746(84)90037-4

Cited by 19 publications

(11 citation statements)

References 17 publications

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“…In contrast, these PGs enhance the production of IL-10 (Harizi et al, 2002). Indeed, overexpression of PGE 2 has been reported in a number of conditions associated with increased susceptibility to infection, including cancer (Starczewski et al, 1984), aging (Hayek et al, 1997) and cystic fibrosis (Medjane et al, 2005; Strandvik et al, 1996). Interestingly, PGE 2 , generated during the onset phase of inflammation, also indirectly elicits pro-resolution actions by switching on the transcription of enzymes required for the biosynthesis of other classes of bioactive lipids that are potent pro-resolution mediators, such as LXs (Levy et al, 2001), resolvins (Rvs) and protectins (PDs) (Hong et al, 2003; Marcheselli et al, 2003; Serhan et al, 2000; Serhan et al, 2002).…”

Section: Resolvins and Protectinsmentioning

confidence: 99%

Proresolving Lipid Mediators and Mechanisms in the Resolution of Acute Inflammation

2014

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SUMMARY Inflammatory responses, like all biological cascades, are shaped by a delicate balance between positive and negative feedback loops. It is now clear that in addition to positive and negative checkpoints, the inflammatory cascade rather unexpectedly boasts an additional checkpoint, a family of chemicals that actively promote resolution and tissue repair without compromising host defence. Indeed the resolution phase of inflammation is just as actively orchestrated and carefully choreographed as its induction and inhibition. In this review we explore the immunological consequences of these omega-3-derived specialized pro-resolving mediators (SPMs) and discuss their place within what is currently understood of the role of the arachidonic acid-derived prostaglandins, lipoxins and their natural C15-epimers. We propose that treatment of inflammation should not be restricted to the use of inhibitors of the acute cascade (antagonism) but broadened to take account of the enormous therapeutic potential of inducers (agonists) of the resolution phase of inflammation.

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Section: Resolvins and Protectinsmentioning

confidence: 99%

Proresolving Lipid Mediators and Mechanisms in the Resolution of Acute Inflammation

2014

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“…Increased plasma PGE 2 levels have been reported in murine models and in patients who have undergone bone marrow transplantation [16, 122], are infected with HIV [123], display protein-calorie malnutrition [124], are smokers, are aging [125], or have cancer [126] or cystic fibrosis [127]. In all circumstances, these conditions are associated with susceptibility to infection.…”

Section: Therapeutic Approachesmentioning

confidence: 99%

Prostaglandin and the Suppression of Phagocyte Innate Immune Responses in Different Organs

Medeiros

Peres‐Buzalaf

Verdan

et al. 2012

Mediators of Inflammation

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The local and systemic production of prostaglandin E2 (PGE2) and its actions in phagocytes lead to immunosuppressive conditions. PGE2 is produced at high levels during inflammation, and its suppressive effects are caused by the ligation of the E prostanoid receptors EP2 and EP4, which results in the production of cyclic AMP. However, PGE2 also exhibits immunostimulatory properties due to binding to EP3, which results in decreased cAMP levels. The various guanine nucleotide-binding proteins (G proteins) that are coupled to the different EP receptors account for the pleiotropic roles of PGE2 in different disease states. Here, we discuss the production of PGE2 and the actions of this prostanoid in phagocytes from different tissues, the relative contribution of PGE2 to the modulation of innate immune responses, and the novel therapeutic opportunities that can be used to control inflammatory responses.

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“…These suppressive actions may help to promote resolution of tissue inflammation once infection has been contained, but enhanced production of PGE 2 could impair innate immunity. Indeed, excessive generation of PGE 2 has been implicated in immunosuppressive states including bone marrow transplantation [29 -31], cancer [32], aging [33], malnutrition [34], and cystic fibrosis [35]. These suppressive actions on macrophages, including AMs, are mediated by ligation of E prostanoid (EP) receptors 2 and 4, which are coupled to a stimulatory G protein ␣-subunit that activates adenylyl cyclase to catalyze the formation of cAMP [36 -39].…”

Section: Introductionmentioning

confidence: 99%

Regulation of alveolar macrophage p40phox: hierarchy of activating kinases and their inhibition by PGE2

Bourdonnay

Serezani

Aronoff

et al. 2012

Journal of Leukocyte Biology

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PGE(2), produced in the lung during infection with microbes such as Klebsiella pneumoniae, inhibits alveolar macrophage (AM) antimicrobial functions by preventing H(2)O(2) production by NADPH oxidase (NADPHox). Activation of the NADPHox complex is poorly understood in AMs, although in neutrophils it is known to be mediated by kinases including PI3K/Akt, protein kinase C (PKC) δ, p21-activated protein kinase (PAK), casein kinase 2 (CK2), and MAPKs. The p40phox cytosolic subunit of NADPHox has been recently recognized to function as a carrier protein for other subunits and a positive regulator of oxidase activation, a role previously considered unique to another subunit, p47phox. The regulation of p40phox remains poorly understood, and the effect of PGE(2) on its activation is completely undefined. We addressed these issues in rat AMs activated with IgG-opsonized K. pneumoniae. The kinetics of kinase activation and the consequences of kinase inhibition and silencing revealed a critical role for a PKCδ-PAK-class I PI3K/Akt1 cascade in the regulation of p40phox activation upon bacterial challenge in AMs; PKCα, ERK, and CK2 were not involved. PGE(2) inhibited the activation of p40phox, and its effects were mediated by protein kinase A type II, were independent of interactions with anchoring proteins, and were directed at the distal class I PI3K/Akt1 activation step. Defining the kinases that control AM p40phox activation and that are the targets for inhibition by PGE(2) provides new insights into immunoregulation in the infected lung.

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Plasma levels of 15-keto-13,14-dihydro-prostaglandin E2 in patients with bronchogenic carcinoma

Cited by 19 publications

References 17 publications

Proresolving Lipid Mediators and Mechanisms in the Resolution of Acute Inflammation

Proresolving Lipid Mediators and Mechanisms in the Resolution of Acute Inflammation

Prostaglandin and the Suppression of Phagocyte Innate Immune Responses in Different Organs

Regulation of alveolar macrophage p40phox: hierarchy of activating kinases and their inhibition by PGE2

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