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Author = PALSSON, EVA;
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Displaying Results 1 - 7 of 7 on page 1 of 1
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Cutting Edge: Mycobacterium tuberculosis Induces Aerobic Glycolysis in Human Alveolar Macrophages That Is Required for Control of Intracellular Bacillary Replication.
(2016)
KEANE, JOSEPH; O'SULLIVAN, MARY; O'NEILL, LUKE; PALSSON, EVA; SHEEDY, FREDERICK
Cutting Edge: Mycobacterium tuberculosis Induces Aerobic Glycolysis in Human Alveolar Macrophages That Is Required for Control of Intracellular Bacillary Replication.
(2016)
KEANE, JOSEPH; O'SULLIVAN, MARY; O'NEILL, LUKE; PALSSON, EVA; SHEEDY, FREDERICK
Abstract:
Recent advances in immunometabolism link metabolic changes in stimulated macrophages to production of IL-1?, a crucial cytokine in the innate immune response to Mycobacterium tuberculosis. To investigate this pathway in the host response to M. tuberculosis, we performed metabolic and functional studies on human alveolar macrophages, human monocyte-derived macrophages, and murine bone marrow?derived macrophages following infection with the bacillus in vitro. M. tuberculosis infection induced a shift from oxidative phosphorylation to aerobic glycolysis in macrophages. Inhibition of this shift resulted in decreased levels of proinflammatory IL-1? and decreased transcription of PTGS2, increased levels of anti-inflammatory IL-10, and increased intracellular bacillary survival. Blockade or absence of IL-1R negated the impact of aerobic glycolysis on intracellular bacillary survival, demonstrating that infection-induced glycolysis limits M. tuberculosis survival in macrophages through indu...
http://hdl.handle.net/2262/77445
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Divergent roles for Ras and Rap in the activation of p38 mitogen-activated protein kinase by interleukin-1
(2000)
O'NEILL, LUKE ANTHONY JOHN; PALSSON, EVA
Divergent roles for Ras and Rap in the activation of p38 mitogen-activated protein kinase by interleukin-1
(2000)
O'NEILL, LUKE ANTHONY JOHN; PALSSON, EVA
Abstract:
peer-reviewed
We have found that lethal toxin from Clostridium sordellii, which specifically inactivates the low molecular weight G proteins Ras, Rap, and Rac, inhibits the activation of p38 mitogen-activated protein kinase (MAPK) by interleukin-1 (IL-1) in EL4.NOB-1 cells and primary fibroblasts. The target protein involved appeared to be Ras, because transient transfections with dominant negative RasN17 inhibited p38 MAPK activation by IL-1. Furthermore, transfections of cells with constitutively active RasVHa-activated p38 MAPK. Further evidence for Ras involvement came from the observation that IL-1 caused a rapid activation of Ras in the cells and from the inhibitory effects of the Ras inhibitors manumycin A and damnacanthal. Toxin B from Clostridium difficile, which inactivates Rac, Cdc42, and Rho, was without effect. Dominant negative versions of Rac (RacN17) or Rap (Rap1AN17) did not inhibit the response. Intriguingly, transfection of cells with dominant negative Rap1AN1...
http://hdl.handle.net/2262/33704
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MyD88 adaptor-like (Mal) functions in the epithelial barrier and contributes to intestinal integrity via protein kinase C
(2014)
CORR, SINEAD; O'NEILL, LUKE; PALSSON, EVA; FALLON, PADRAIC
MyD88 adaptor-like (Mal) functions in the epithelial barrier and contributes to intestinal integrity via protein kinase C
(2014)
CORR, SINEAD; O'NEILL, LUKE; PALSSON, EVA; FALLON, PADRAIC
Abstract:
The prognosis of epithelial ovarian cancer is poor in part due to the high frequency of chemoresistance. Recent evidence points to the Toll-like receptor-4 (TLR4), and particularly its adaptor protein MyD88, as one potential mediator of this resistance. This study aims to provide further evidence that MyD88 positive cancer cells are clinically significant, stem-like and reproducibly detectable for the purposes of prognostic stratification. Expression of TLR4 and MyD88 was assessed immunohistochemically in 198 paraffin-embedded ovarian tissues and in an embryonal carcinoma model of cancer stemness. In parallel, expression of TLR4 and MyD88 mRNA and regulatory microRNAs (miR-21 and miR-146a) was assessed, as well as in a series of chemosensitive and resistant cancer cells lines. Functional analysis of the pathway was assessed in chemoresistant SKOV-3 ovarian cancer cells. TLR4 and MyD88 expression can be reproducibly assessed via immunohistochemistry using a semi-quantitative scoring ...
http://hdl.handle.net/2262/75436
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Pyruvate Kinase M2 Regulates Hif-1alfa Activity and IL-1? Induction and Is a Critical Determinant of the Warburg Effect in LPS-Activated Macrophages.
(2015)
KEANE, JOSEPH; PALSSON, EVA; O'NEILL, LUKE; SHEEDY, FREDERICK
Pyruvate Kinase M2 Regulates Hif-1alfa Activity and IL-1? Induction and Is a Critical Determinant of the Warburg Effect in LPS-Activated Macrophages.
(2015)
KEANE, JOSEPH; PALSSON, EVA; O'NEILL, LUKE; SHEEDY, FREDERICK
Abstract:
TLR4-activated macrophages switch their metabolism from oxidative phosphorylation to glycolysis to rapidly provide for the high energy and biosynthetic demands of infection or injury response. Palsson-McDermott identify PKM2 as a critical modulator of IL-1 b production and the Warburg effect in LPS-activated macrophages, highlighting it as a target in cancer and inflammation
http://hdl.handle.net/2262/73269
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Signal transduction by the lipopolysaccharide receptor, Toll-like receptor-4
(2004)
O'NEILL, LUKE ANTHONY JOHN; PALSSON, EVA
Signal transduction by the lipopolysaccharide receptor, Toll-like receptor-4
(2004)
O'NEILL, LUKE ANTHONY JOHN; PALSSON, EVA
Abstract:
peer-reviewed
An understanding of lipopolysaccharide (LPS) signal transduction is a key goal in the effort to provide a molecular basis for the lethal effect of LPS during septic shock and point the way to novel therapies. Rapid progress in this field during the last 6 years has resulted in the discovery of not only the receptor for LPS ? Toll-like receptor 4 (TLR4) ? but also in a better appreciation of the complexity of the signalling pathways activated by LPS. Soon after the discovery of TLR4, the formation of a receptor complex in response to LPS, consisting of dimerized TLR4 and MD-2, was described. Intracellular events following the formation of this receptor complex depend on different sets of adapters. An early response, which is dependent on MyD88 and MyD88-like adapter (Mal), leads to the activation of nuclear factor-?B (NF-?B). A later response to LPS makes use of TIR-domain-containing adapter-inducing interferon-? (TRIF) and TRIF-related adapter molecule (TRAM), and ...
http://hdl.handle.net/2262/33448
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Succinate is an inflammatory signal that induces IL-1 beta through HIF-1 alpha
(2013)
MCGETTRICK-DILLON, ANNE; CORR, SINEAD; PALSSON, EVA; KELLY, VINCENT; O'NEILL, LUKE
Succinate is an inflammatory signal that induces IL-1 beta through HIF-1 alpha
(2013)
MCGETTRICK-DILLON, ANNE; CORR, SINEAD; PALSSON, EVA; KELLY, VINCENT; O'NEILL, LUKE
Abstract:
Macrophages activated by the Gram-negative bacterial product lipopolysaccharide switch their core metabolism from oxidative phosphorylation to glycolysis. Here we show that inhibition of glycolysis with 2-deoxyglucose suppresses lipopolysaccharide-induced interleukin-1? but not tumour-necrosis factor-? in mouse macrophages. A comprehensive metabolic map of lipopolysaccharide-activated macrophages shows upregulation of glycolytic and downregulation of mitochondrial genes, which correlates directly with the expression profiles of altered metabolites. Lipopolysaccharide strongly increases the levels of the tricarboxylic-acid cycle intermediate succinate. Glutamine-dependent anerplerosis is the principal source of succinate, although the 'GABA (?-aminobutyric acid) shunt' pathway also has a role. Lipopolysaccharide-induced succinate stabilizes hypoxia-inducible factor-1?, an effect that is inhibited by 2-deoxyglucose, with interleukin-1? as an important target. Lipopolysacchar...
http://hdl.handle.net/2262/72421
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Trif-related adapter molecule is phosphorylated by protein kinase C epsilon during Toll-like receptor 4 signalling
(2006)
MCGETTRICK-DILLON, ANNE; O'NEILL, LUKE ANTHONY JOHN; PALSSON, EVA
Trif-related adapter molecule is phosphorylated by protein kinase C epsilon during Toll-like receptor 4 signalling
(2006)
MCGETTRICK-DILLON, ANNE; O'NEILL, LUKE ANTHONY JOHN; PALSSON, EVA
Abstract:
peer-reviewed
PKC? has been shown to play a key role in the effect of the Gram-negative bacterial product LPS; however, the target for PKC? in LPS signaling is unknown. LPS signaling is mediated by Toll-like receptor 4, which uses four adapter proteins, MyD88, MyD88 adapter-like (Mal), Toll/IL-1R domain-containing adapter inducing IFN-? (Trif), and Trif-related adapter molecule (TRAM). Here we show that TRAM is transiently phosphorylated by PKC? on serine-16 in an LPS-dependent manner. Activation of IFN regulatory factor 3 and induction of the chemokine RANTES, which are both TRAM-dependent, were attenuated in PKC?-deficient cells. TRAMS16A is inactive when overexpressed and is attenuated in its ability to reconstitute signaling in TRAM-deficient cells. We have therefore uncovered a key process in Toll-like receptor 4 signaling, identifying TRAM as the target for PKC?.
http://hdl.handle.net/2262/33442
Displaying Results 1 - 7 of 7 on page 1 of 1
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