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

Sent on Thursday, 2011 Aug 04
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 - 8 of 8

1.	Science. 2011 Jul 22;333(6041):411-2. Evolution. Seeing the trees in your terrace. Kubatko LS, Pearl DK. Source Department of Statistics, The Ohio State University, Columbus, OH 43210, USA. lkubatko@stat.osu.edu Comment on Science. 2011 Jul 22;333(6041):448-50.
	PMID: 21778387 [PubMed - indexed for MEDLINE]
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2.	Science. 2011 Jul 22;333(6041):405; author reply 405. Comment on "Activation of β-catenin in dendritic cells r egulates immunity versus tolerance in the intestine". Murphy KM. Source Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. kmurphy@wustl.edu Comment on Science. 2010 Aug 13;329(5993):849-53. Abstract Manicassamy et al. (Reports, 13 August 2010, p. 849) deleted β-catenin in intestinal immune cells using a CD11c-driven Cre recombinase, which decreased anti-inflammatory mediators and increased inflammatory bowel disease. However, the deletion of β-catenin in macrophages remains a caveat to their interpretation that Wnt signaling programs dendritic cells into a tolerogenic state. Development of strains expressing Cre in a more finely lineage-restricted pattern may help resolve this issue. Free Article
	PMID: 21778384 [PubMed - indexed for MEDLINE]
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3.	Nature. 2011 Jul 17;475(7357):514-8. doi: 10.1038/nature10228. Control of TH17 cells occurs in the smal l intestine. Esplugues E, Huber S, Gagliani N, Hauser AE, Town T, Wan YY, O'Connor W Jr, Rongvaux A, Van Rooijen N, Haberman AM, Iwakura Y, Kuchroo VK, Kolls JK, Bluestone JA, Herold KC, Flavell RA. Source Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA. enric.esplugues@yale.edu Abstract Interleukin (IL)-17-producing T helper cells (T(H)17) are a recently identified CD4(+) T cell subset distinct from T helper type 1 (T(H)1) and T helper type 2 (T(H)2) cells. T(H)17 cells can drive antigen-specific autoimmune diseases and are considered the main population of pathogenic T cells driving experimental autoimmune encephalomyelitis (EAE), the mouse model for multiple sclerosis. The factors that are needed for the generation of T(H)17 cells have been well characterized. However, where and how the immune system controls T(H)17 cells in vivo remains unclear. Here, by using a model of tolerance induced by CD3-specific antibody, a model of sepsis and influenza A viral infection (H1N1), we show that pro-inflammatory T(H)17 cells can be redirected to and controlled in the small intestine. T(H)17-specific IL-17A secretion induced expression of the chemokine CCL20 in the small intestine, facilitating the migration of these cells specifically to the small intestine via the CCR6/CCL20 axis. Moreover, we found that T(H)17 cells are controlled by two different mechanisms in the small intestine: first, they are eliminated via the intestinal lumen; second, pro-inflammatory T(H)17 cells simultaneously acquire a regulatory phenotype with in vitro and in vivo immune-suppressive properties (rT(H)17). These results identify mechanisms limiting T(H)17 cell pathogenicity and implicate the gastrointestinal tract as a site for control of T(H)17 cells. PMCID: PMC3148838 [Available on 2012/1/28]
	PMID: 21765430 [PubMed - indexed for MEDLINE]
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4.	Nature. 2011 Jul 13;475(7357):493-6. doi: 10.1038/nature10231. Inference of human population history from individual whole-genome sequences. Li H, Durbin R. Source The Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK. Abstract The history of human population size is important for understanding human evolution. Various studies have found evidence for a founder event (bottleneck) in East Asian and European populations, associated with the human dispersal out-of-Africa event around 60 thousand years (kyr) ago. However, these studies have had to assume simplified demographic models with few parameters, and they do not provide a precise date for the start and stop times of the bottleneck. Here, with fewer assumptions on population size changes, we present a more detailed history of human population sizes between approximately ten thousand and a million years ago, using the pairwise sequentially Markovian coalescent model applied to the complete diploid genome sequences of a Chinese male (YH), a Korean male (SJK), three European individuals (J. C. Venter, NA12891 and NA12878 (ref. 9)) and two Yoruba males (NA18507 (ref. 10) and NA19239). We infer that European and Chinese populations had very similar population-size histories before 10-20 kyr ago. Both populations experienced a severe bottleneck 10-60 kyr ago, whereas African populations experienced a milder bottleneck from which they recovered earlier. All three populations have an elevated effective population size between 60 and 250 kyr ago, possibly due to population substructure. We also infer that the differentiation of genetically modern humans may have started as early as 100-120 kyr ago, but considerable genetic exchanges may still have occurred until 20-40 kyr ago.
	PMID: 21753753 [PubMed - indexed for MEDLINE]
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5.	Nature. 2011 Jul 6;475(7357):506-9. doi: 10.1038/nature10307. Legionella pneumophila SidD is a deAMPylase that modifies Rab1. Tan Y, Luo ZQ. Source Department of Biological Sciences, Purdue University, 915 West State Street, West Lafayette, Indiana 47907, USA. Abstract Legionella pneumophila actively modulates host vesicle trafficking pathways to facilitate its intracellular replication with effectors translocated by the Dot/Icm type IV secretion system (T4SS). The SidM/DrrA protein functions by locking the small GTPase Rab1 into an active form by its guanine nucleotide exchange factor (GEF) and AMPylation activity. Here we demonstrate that the L. pneumophila protein SidD preferably deAMPylates Rab1. We found that the deAMPylation activity of SidD could suppress the toxicity of SidM to yeast and is required to release Rab1 from bacterial phagosomes efficiently. A molecular mechanism for the temporal control of Rab1 activity in different phases of L. pneumophila infection is thus established. These observations indicate that AMPylation-mediated signal transduction is a reversible process regulated by specific enzymes. PMCID: PMC3146296 [Available on 2012/1/28]
	PMID: 21734656 [PubMed - indexed for MEDLINE]
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6.	Science. 2011 Jul 22;333(6041):453-6. Epub 2011 Jun 16. De-AMPylation of the small GTPase Rab1 by the pathogen Legionella pneumophila. Neunuebel MR, Chen Y, Gaspar AH, Backlund PS Jr, Yergey A, Machner MP. Source Cell Biology and Metabolism Program, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA. Abstract The bacterial pathogen Legionella pneumophila exploits host cell vesicle transport by transiently manipulating the activity of the small guanosine triphosphatase (GTPase) Rab1. The effector protein SidM recruits Rab1 to the Legionella-containing vacuole (LCV), where it activates Rab1 and then AMPylates it by covalently adding adenosine monophosphate (AMP). L. pneumophila GTPase-activating protein LepB inactivates Rab1 before its removal from LCVs. Because LepB cannot bind AMPylated Rab1, the molecular events leading to Rab1 inactivation are unknown. We found that the effector protein SidD from L. pneumophila catalyzed AMP release from Rab1, generating de-AMPylated Rab1 accessible for inactivation by LepB. L. pneumophila mutants lacking SidD were defective for Rab1 removal from LCVs, identifying SidD as the missing link connecting the processes of early Rab1 accumulation and subsequent Rab1 removal during infection.
	PMID: 21680813 [PubMed - indexed for MEDLINE]
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7.	Science. 2011 Jul 22;333(6041):448-50. Epub 2011 Jun 16. Terraces in phylogenetic tree space. Sanderson MJ, McMahon MM, Steel M. Source Department of Ecology and Evolutionary Biology, University of Arizona, Tucson, AZ 85721, USA. sanderm@email.arizona.edu Comment in Science. 2011 Jul 22;333(6041):411-2. Abstract A key step in assembling the tree of life is the construction of species-rich phylogenies from multilocus--but often incomplete--sequence data sets. We describe previously unknown structure in the landscape of solutions to the tree reconstruction problem, comprising sometimes vast "terraces" of trees with identical quality, arranged on islands of phylogenetically similar trees. Phylogenetic ambiguity within a terrace can be characterized efficiently and then ameliorated by new algorithms for obtaining a terrace's maximum-agreement subtree or by identifying the smallest set of new targets for additional sequencing. Algorithms to find optimal trees or estimate Bayesian posterior tree distributions may need to navigate strategically in the neighborhood of large terraces in tree space.
	PMID: 21680810 [PubMed - indexed for MEDLINE]
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8.	PLoS One. 2011 Jan 7;6(1):e15723. Macrophage activation and differentiation signals regulate schlafen-4 gene expr ession: evidence for Schlafen-4 as a modulator of myelopoiesis. van Zuylen WJ, Garceau V, Idris A, Schroder K, Irvine KM, Lattin JE, Ovchinnikov DA, Perkins AC, Cook AD, Hamilton JA, Hertzog PJ, Stacey KJ, Kellie S, Hume DA, Sweet MJ. Source The University of Queensland, Institute for Molecular Bioscience, Queensland, Australia. Abstract BACKGROUND: The ten mouse and six human members of the Schlafen (Slfn) gene family all contain an AAA domain. Little is known of their function, but previous studies suggest roles in immune cell development. In this report, we assessed Slfn regulation and function in macrophages, which are key cellular regulators of innate immunity. METHODOLOGY/PRINCIPAL FINDINGS: Multiple members of the Slfn family were up-regulated in mouse bone marrow-derived macrophages (BMM) by the Toll-like Receptor (TLR)4 agonist lipopolysaccharide (LPS), the TLR3 agonist Poly(I∶C), and in disease-affected joints in the collagen-induced model of rheumatoid arthritis. Of these, the most inducible was Slfn4. TLR agonists that signal exclusively through the MyD88 adaptor protein had more modest effects on Slfn4 mRNA levels, thus implicating MyD88-independent signalling and autocrine interferon (IFN)-β in inducible expression. This was supported by the substantial reduction in basal and LPS-induced Slfn4 mRNA expression in IFNAR-1⁻/⁻ BMM. LPS causes growth arrest in macrophages, and other Slfn family genes have been implicated in growth control. Slfn4 mRNA levels were repressed during macrophage colony-stimulating factor (CSF-1)-mediated differentiation of bone marrow progenitors into BMM. To determine the role of Slfn4 in vivo, we over-expressed the gene specifically in macrophages in mice using a csf1r promoter-driven binary expression system. Transgenic over-expression of Slfn4 in myeloid cells did not alter macrophage colony formation or proliferation in vitro. Monocyte numbers, as well as inflammatory macrophages recruited to the peritoneal cavity, were reduced in transgenic mice that specifically over-expressed Slfn4, while macrophage numbers and hematopoietic activity were increased in the livers and spleens. CONCLUSIONS: Slfn4 mRNA levels were up-regulated during macrophage activation but down-regulated during differentiation. Constitutive Slfn4 expression in the myeloid lineage in vivo perturbs myelopoiesis. We hypothesise that the down-regulation of Slfn4 gene expression during macrophage differentiation is a necessary step in development of this lineage. PMCID: PMC3017543 Free PMC Article
	PMID: 21249125 [PubMed - indexed for MEDLINE]
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