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

Sent on Friday, 2014 May 30
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 - 3 of 3

1.	Nat Med. 2014 Apr;20(4):335-7. doi: 10.1038/nm.3526. Hypoferremia of infection: a double-edged sword? Lokken KL, Tsolis RM, Bäumler AJ. Author information: Department of Medical Microbiology and Immunology, School of Medicine, University of California-Davis, Davis, California, USA.
	PMID: 24710374 [PubMed - indexed for MEDLINE]
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2.	Nat Med. 2014 Apr;20(4):419-24. doi: 10.1038/nm.3483. Epub 2014 Mar 23. Inverse agonist of estrogen-related receptor γ controls Salmonella typhimurium infection by modulating host iron homeostasis. Kim DK1, Jeong JH2, Lee JM3, Kim KS4, Park SH5, Kim YD3, Koh M6, Shin M3, Jung YS3, Kim HS7, Lee TH8, Oh BC9, Kim JI10, Park HT11, Jeong WI12, Lee CH13, Park SB14, Min JJ15, Jung SI16, Choi SY17, Choy HE4, Choi HS3. Author information: 11] National Creative Research Initiatives Center for Nuclear Receptor Signals and Hormone Research Center, School of Biological Sciences and Technology, Chonnam National University, Gwangju, Republic of Korea. [2]. 21] Department of Microbiology, Chonnam National University Medical School, Gwangju, Republic of Korea. [2] Department of Molecular Medicine(BK21plus), Chonnam National University Graduate School, Gwangju, Republic of Korea. [3]. 3National Creative Research Initiatives Center for Nuclear Receptor Signals and Hormone Research Center, School of Biological Sciences and Technology, Chonnam National University, Gwangju, Republic of Korea. 41] Department of Microbiology, Chonnam National University Medical School, Gwangju, Republic of Korea. [2] Department of Molecular Medicine(BK21plus), Chonnam National University Graduate School, Gwangju, Republic of Korea. 5Department of Nuclear Medicine, Chonnam National University Medical School, Gwangju, Republic of Korea. 6Department of Chemistry, College of Natural Sciences, Seoul National University, Seoul, Republic of Korea. 7Department of Forensic Medicine, Chonnam National University Medical School, Gwangju, Republic of Korea. 81] Department of Molecular Medicine(BK21plus), Chonnam National University Graduate School, Gwangju, Republic of Korea. [2] Department of Oral Biochemistry, Dental Science Research Institute, Chonnam National University, Gwangju, Republic of Korea. 9Lee Gil Ya Cancer and Diabetes Institute, Gachon University Graduate School of Medicine, Incheon, Republic of Korea. 101] School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju, Republic of Korea. [2] AnyGen, Jeonnam NanoBioResearch Center, Jangseong-gun, Republic of Korea. 11Department of Physiology, Mitochondria Hub Regulation Center, College of Medicine, Dong-A University, Busan, Republic of Korea. 12Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon, Republic of Korea. 13Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea. 141] Department of Chemistry, College of Natural Sciences, Seoul National University, Seoul, Republic of Korea. [2] Department of Biophysics and Chemical Biology, College of Natural Sciences, Seoul National University, Seoul, Republic of Korea. 151] Department of Molecular Medicine(BK21plus), Chonnam National University Graduate School, Gwangju, Republic of Korea. [2] Department of Nuclear Medicine, Chonnam National University Medical School, Gwangju, Republic of Korea. 161] Department of Molecular Medicine(BK21plus), Chonnam National University Graduate School, Gwangju, Republic of Korea. [2] Department of Infectious Diseases, Chonnam National University Medical School, Gwangju, Republic of Korea. 17Department of Biomedical Sciences, Chonnam National University Medical School, Gwangju, Republic of Korea. Abstract In response to microbial infection, expression of the defensin-like peptide hepcidin (encoded by Hamp) is induced in hepatocytes to decrease iron release from macrophages. To elucidate the mechanism by which Salmonella enterica var. Typhimurium (S. typhimurium), an intramacrophage bacterium, alters host iron metabolism for its own survival, we examined the role of nuclear receptor family members belonging to the NR3B subfamily in mouse hepatocytes. Here, we report that estrogen-related receptor γ (ERRγ, encoded by Esrrg) modulates the intramacrophage proliferation of S. typhimurium by altering host iron homeostasis, and we demonstrate an antimicrobial effect of an ERRγ inverse agonist. Hepatic ERRγ expression was induced by S. typhimurium-stimulated interleukin-6 signaling, resulting in an induction of hepcidin and eventual hypoferremia in mice. Conversely, ablation of ERRγ mRNA expression in liver attenuated the S. typhimurium-mediated induction of hepcidin and normalized the hypoferremia caused by S. typhimurium infection. An inverse agonist of ERRγ ameliorated S. typhimurium-mediated hypoferremia through reduction of ERRγ-mediated hepcidin mRNA expression and exerted a potent antimicrobial effect on the S. typhimurium infection, thereby improving host survival. Taken together, these findings suggest an alternative approach to control multidrug-resistant intracellular bacteria by modulating host iron homeostasis.
	PMID: 24658075 [PubMed - indexed for MEDLINE]
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3.	Nat Med. 2014 Apr;20(4):377-84. doi: 10.1038/nm.3467. Epub 2014 Mar 2. Netrin-1 promotes adipose tissue macrophage retention and insulin resistance in obesity. Ramkhelawon B1, Hennessy EJ1, Ménager M2, Ray TD1, Sheedy FJ1, Hutchison S1, Wanschel A1, Oldebeken S1, Geoffrion M3, Spiro W1, Miller G4, McPherson R4, Rayner KJ4, Moore KJ1. Author information: 1Department of Medicine, Marc and Ruti Bell Program for Vascular Biology and Disease, The Leon H. Charney Division of Cardiology, New York University School of Medicine, New York, New York, USA. 2Molecular Pathogenesis Program, The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York, New York, USA. 3University of Ottawa Heart Institute, Ottawa, Ontario, Canada. 4Department of Surgery, New York University School of Medicine, New York, New York, USA. Abstract During obesity, macrophage accumulation in adipose tissue propagates the chronic inflammation and insulin resistance associated with type 2 diabetes. The factors, however, that regulate the accrual of macrophages in adipose tissue are not well understood. Here we show that the neuroimmune guidance cue netrin-1 is highly expressed in obese but not lean adipose tissue of humans and mice, where it directs the retention of macrophages. Netrin-1, whose expression is induced in macrophages by the saturated fatty acid palmitate, acts via its receptor Unc5b to block their migration. In a mouse model of diet-induced obesity, we show that adipose tissue macrophages exhibit reduced migratory capacity, which can be restored by blocking netrin-1. Furthermore, hematopoietic deletion of Ntn1 facilitates adipose tissue macrophage emigration, reduces inflammation and improves insulin sensitivity. Collectively, these findings identify netrin-1 as a macrophage retention signal in adipose tissue during obesity that promotes chronic inflammation and insulin resistance. PMCID: PMC3981930 [Available on 2014/10/1]
	PMID: 24584118 [PubMed - indexed for MEDLINE]
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