What's new for 'JKB_daily1' in PubMed

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

Sent on Friday, 2015 February 20
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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PubMed Results

Items 1 - 5 of 5

1.	Science. 2015 Feb 6;347(6222):667-72. doi: 10.1126/science.aaa1300. Host response. Inflammation-induced disruption of SCS macrophages impairs B cell responses to secondary infection. Gaya M1, Castello A1, Montaner B1, Rogers N2, Reis e Sousa C2, Bruckbauer A1, Batista FD3. Author information: 1Lymphocyte Interaction Laboratory, London Research Institute, Cancer Research UK, 44 Lincoln's Inn Fields, London WC2A 3LY, UK. 2Immunobiology Laboratory, London Research Institute, Cancer Research UK, 44 Lincoln's Inn Fields, London WC2A 3LY, UK. 3Lymphocyte Interaction Laboratory, London Research Institute, Cancer Research UK, 44 Lincoln's Inn Fields, London WC2A 3LY, UK. facundo.batista@cancer.org.uk. Comment in Immunology. There goes the macrophage neighborhood. [Science. 2015] Abstract The layer of macrophages at the subcapsular sinus (SCS) captures pathogens entering the lymph node, preventing their global dissemination and triggering an immune response. However, how infection affects SCS macrophages remains largely unexplored. Here we show that infection and inflammation disrupt the organization of SCS macrophages in a manner that involves the migration of mature dendritic cells to the lymph node. This disrupted organization reduces the capacity of SCS macrophages to retain and present antigen in a subsequent secondary infection, resulting in diminished B cell responses. Thus, the SCS macrophage layer may act as a sensor or valve during infection to temporarily shut down the lymph node to further antigenic challenge. This shutdown may increase an organism's susceptibility to secondary infections. Copyright © 2015, American Association for the Advancement of Science.
	PMID: 25657250 [PubMed - indexed for MEDLINE]
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2.	Science. 2015 Feb 6;347(6222):609-10. doi: 10.1126/science.aaa6919. Immunology. There goes the macrophage neighborhood. Hickman HD1. Author information: 1National Institutes of Health, Bethesda, MD, USA. hhickman@mail.nih.gov. Comment on Host response. Inflammation-induced disruption of SCS macrophages impairs B cell responses to secondary infection. [Science. 2015]
	PMID: 25657230 [PubMed - indexed for MEDLINE]
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3.	Nature. 2015 Jan 8;517(7533):170-3. doi: 10.1038/nature14029. Glutathione activates virulence gene expression of an intracellular pathogen. Reniere ML1, Whiteley AT2, Hamilton KL3, John SM1, Lauer P4, Brennan RG3, Portnoy DA5. Author information: 1Department of Molecular and Cell Biology, University of California, Berkeley, California 94720, USA. 2Graduate Group in Infectious Diseases and Immunity, School of Public Health, University of California, Berkeley, California 94720, USA. 3Department of Biochemistry, Duke University School of Medicine, Durham, North Carolina 27710, USA. 4Aduro BioTech, Inc. Berkeley, California 94710, USA. 51] Department of Molecular and Cell Biology, University of California, Berkeley, California 94720, USA [2] School of Public Health, University of California, Berkeley, California 94720, USA. Abstract Intracellular pathogens are responsible for much of the world-wide morbidity and mortality due to infectious diseases. To colonize their hosts successfully, pathogens must sense their environment and regulate virulence gene expression appropriately. Accordingly, on entry into mammalian cells, the facultative intracellular bacterial pathogen Listeria monocytogenes remodels its transcriptional program by activating the master virulence regulator PrfA. Here we show that bacterial and host-derived glutathione are required to activate PrfA. In this study a genetic selection led to the identification of a bacterial mutant in glutathione synthase that exhibited reduced virulence gene expression and was attenuated 150-fold in mice. Genome sequencing of suppressor mutants that arose spontaneously in vivo revealed a single nucleotide change in prfA that locks the protein in the active conformation (PrfA*) and completely bypassed the requirement for glutathione during infection. Biochemical and genetic studies support a model in which glutathione-dependent PrfA activation is mediated by allosteric binding of glutathione to PrfA. Whereas glutathione and other low-molecular-weight thiols have important roles in redox homeostasis in all forms of life, here we demonstrate that glutathione represents a critical signalling molecule that activates the virulence of an intracellular pathogen. PMCID: PMC4305340 [Available on 2015-07-08]
	PMID: 25567281 [PubMed - indexed for MEDLINE]
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4.	Nature. 2015 Jan 8;517(7533):128-9. doi: 10.1038/517128a. End of cancer-genome project prompts rethink. Ledford H.
	PMID: 25567260 [PubMed - indexed for MEDLINE]
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5.	Lancet. 2014 Nov 22;384(9957):1900. doi: 10.1016/S0140-6736(14)61645-7. Epub 2014 Nov 21. A pregnant woman with chronic meningococcaemia from Neisseria meningitidis with lpxL1-mutations. Persa OD1, Jazmati N2, Robinson N3, Wolke M2, Kremer K4, Schweer K5, Plum G2, Schlaak M4. Author information: 1Department of Dermatology and Venereology, University of Cologne, Cologne, Germany. Electronic address: oana-diana.persa@uk-koeln.de. 2Institute for Medical Microbiology, Immunology and Hygiene, University of Cologne, Cologne, Germany. 3Institute for Medical Microbiology, Immunology and Hygiene, University of Cologne, Cologne, Germany; CECAD Research Center, Cologne, Germany. 4Department of Dermatology and Venereology, University of Cologne, Cologne, Germany. 5Department I of Internal Medicine, Division of Infectious Diseases, University of Cologne, Cologne, Germany.
	PMID: 25457917 [PubMed - indexed for MEDLINE]
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