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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Thursday, 2014 September 18
Search: (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))

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1.	Nature. 2014 Jul 10;511(7508):167-76. doi: 10.1038/nature13312. Metabolism of stromal and immune cells in health and disease. Ghesquière B, Wong BW, Kuchnio A, Carmeliet P. Author information: 1] Laboratory of Angiogenesis and Neurovascular Link, Vesalius Research Center, Department of Oncology, University of Leuven, Leuven B-3000, Belgium [2] Laboratory of Angiogenesis and Neurovascular Link, Vesalius Research Center, VIB, Leuven B-3000, Belgium. Abstract Cancer cells have been at the centre of cell metabolism research, but the metabolism of stromal and immune cells has received less attention. Nonetheless, these cells influence the progression of malignant, inflammatory and metabolic disorders. Here we discuss the metabolic adaptations of stromal and immune cells in health and disease, and highlight how metabolism determines their differentiation and function.
	PMID: 25008522 [PubMed - indexed for MEDLINE]
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2.	Nature. 2014 Jul 10;511(7508):184-90. doi: 10.1038/nature13323. Aryl hydrocarbon receptor control of a disease tolerance defence pathway. Bessede A1, Gargaro M2, Pallotta MT3, Matino D3, Servillo G3, Brunacci C3, Bicciato S4, Mazza EM4, Macchiarulo A5, Vacca C3, Iannitti R3, Tissi L3, Volpi C3, Belladonna ML3, Orabona C3, Bianchi R3, Lanz TV6, Platten M6, Della Fazia MA3, Piobbico D3, Zelante T3, Funakoshi H7, Nakamura T8, Gilot D9, Denison MS10, Guillemin GJ11, DuHadaway JB12, Prendergast GC12, Metz R13, Geffard M14, Boon L15, Pirro M16, Iorio A17, Veyret B14, Romani L3, Grohmann U3, Fallarino F3, Puccetti P3. Author information: 11] Department of Experimental Medicine, University of Perugia, 06132 Perugia, Italy [2] IMS Laboratory, University of Bordeaux, 33607 Pessac, France [3]. 21] Department of Experimental Medicine, University of Perugia, 06132 Perugia, Italy [2]. 3 Department of Experimental Medicine, University of Perugia, 06132 Perugia, Italy. 4Center for Genome Research, University of Modena and Reggio Emilia, 41125 Modena, Italy. 5Department of Chemistry and Technology of Drugs, University of Perugia, 06123 Perugia, Italy. 61] Experimental Neuroimmunology Unit, German Cancer Research Center, 69120 Heidelberg, Germany [2] Department of Neurooncology, University Hospital, 69120 Heidelberg, Germany. 7Center for Advanced Research and Education, Asahikawa Medical University, 078-8510 Asahikawa, Japan. 8Kringle Pharma Joint Research Division for Regenerative Drug Discovery, Center for Advanced Science and Innovation, Osaka University, 565-0871 Osaka, Japan. 9CNRS UMR6290, Institut de Génétique et Développement de Rennes, Université de Rennes 1, 35043 Rennes, France. 10Department of Environmental Toxicology, University of California, Davis, 95616 California, USA. 11Australian School of Advanced Medicine (ASAM), Macquarie University, 2109 New South Wales, Australia. 12Lankenau Institute for Medical Research, Wynnewood, 19096 Pennsylvania, USA. 13New Link Genetics Corporation, Ames, 50010 Iowa, USA. 14IMS Laboratory, University of Bordeaux, 33607 Pessac, France. 15Bioceros, 3584 Utrecht, The Netherlands. 16Department of Medicine, University of Perugia, 06132 Perugia, Italy. 17Department of Clinical Epidemiology & Biostatistics, McMaster University, Ontario L8S 4K1, Canada. Abstract Disease tolerance is the ability of the host to reduce the effect of infection on host fitness. Analysis of disease tolerance pathways could provide new approaches for treating infections and other inflammatory diseases. Typically, an initial exposure to bacterial lipopolysaccharide (LPS) induces a state of refractoriness to further LPS challenge (endotoxin tolerance). We found that a first exposure of mice to LPS activated the ligand-operated transcription factor aryl hydrocarbon receptor (AhR) and the hepatic enzyme tryptophan 2,3-dioxygenase, which provided an activating ligand to the former, to downregulate early inflammatory gene expression. However, on LPS rechallenge, AhR engaged in long-term regulation of systemic inflammation only in the presence of indoleamine 2,3-dioxygenase 1 (IDO1). AhR-complex-associated Src kinase activity promoted IDO1 phosphorylation and signalling ability. The resulting endotoxin-tolerant state was found to protect mice against immunopathology in Gram-negative and Gram-positive infections, pointing to a role for AhR in contributing to host fitness. PMCID: PMC4098076 [Available on 2015/2/10]
	PMID: 24930766 [PubMed - indexed for MEDLINE]
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