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Medical Forum / General / Nutrition / November 2004Iron / infection
Nature. 2004 Nov 7 [Epub ahead of print] Links Lipocalin 2 mediates an innate immune response to bacterial infection by sequestrating iron. Flo TH, Smith KD, Sato S, Rodriguez DJ, Holmes MA, Strong RK, Akira S, Aderem A. [1] Institute for Systems Biology, Seattle, Washington 98103, USA [2] Institute for Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, 7489 Trondheim, Norway [3] These authors contributed equally to this work. Although iron is required to sustain life, its free concentration and metabolism have to be tightly regulated. This is achieved through a variety of iron-binding proteins including transferrin and ferritin. During infection, bacteria acquire much of their iron from the host by synthesizing siderophores that scavenge iron and transport it into the pathogen. We recently demonstrated that enterochelin, a bacterial catecholate siderophore, binds to the host protein lipocalin 2 (ref. 5). Here, we show that this event is pivotal in the innate immune response to bacterial infection. Upon encountering invading bacteria the Toll-like receptors on immune cells stimulate the transcription, translation and secretion of lipocalin 2; secreted lipocalin 2 then limits bacterial growth by sequestrating the iron-laden siderophore. Our finding represents a new component of the innate immune system and the acute phase response to infection. PMID: 15531878 [PubMed - as supplied by publisher] -------------------------------------------------------------------------- ------ Who loves ya. Tom  SignatureJesus Was A Vegetarian! http://jesuswasavegetarian.7h.com Man Is A Herbivore! http://pages.ivillage.com/ironjustice/manisaherbivore DEAD PEOPLE WALKING http://pages.ivillage.com/ironjustice/deadpeoplewalking "Although iron is required to sustain life, its free concentration and metabolism have to be tightly regulated. This is achieved through a variety of iron-binding proteins including transferrin and ferritin." Contridicts core of iron causes all disease thesis,ie. iron is not controled and we must avoid consuming it and use methods to reduce it. >Subject: Re: Iron / infection >From: markd@toad-net.com [quoted text clipped - 8 lines] >Contridicts core of iron causes all disease thesis,ie. iron is not >controled and we must avoid consuming it and use methods to reduce it. Comments from .. markd . noted .. and filed .. Nature. 2004 Nov 7 [Epub ahead of print] Links Lipocalin 2 mediates an innate immune response to bacterial infection by sequestrating iron. Flo TH, Smith KD, Sato S, Rodriguez DJ, Holmes MA, Strong RK, Akira S, Aderem A. [1] Institute for Systems Biology, Seattle, Washington 98103, USA [2] Institute for Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, 7489 Trondheim, Norway [3] These authors contributed equally to this work. Although iron is required to sustain life, its free concentration and metabolism have to be tightly regulated. This is achieved through a variety of iron-binding proteins including transferrin and ferritin. During infection, bacteria acquire much of their iron from the host by synthesizing siderophores that scavenge iron and transport it into the pathogen. We recently demonstrated that enterochelin, a bacterial catecholate siderophore, binds to the host protein lipocalin 2 (ref. 5). Here, we show that this event is pivotal in the innate immune response to bacterial infection. Upon encountering invading bacteria the Toll-like receptors on immune cells stimulate the transcription, translation and secretion of lipocalin 2; secreted lipocalin 2 then limits bacterial growth by sequestrating the iron-laden siderophore. Our finding represents a new component of the innate immune system and the acute phase response to infection. PMID: 15531878 [PubMed - as supplied by publisher] -------------------------------------------------------------------------- ------ Who loves ya. Tom SignatureJesus Was A Vegetarian! http://jesuswasavegetarian.7h.com Man Is A Herbivore! http://pages.ivillage.com/ironjustice/manisaherbivore DEAD PEOPLE WALKING http://pages.ivillage.com/ironjustice/deadpeoplewalking Several contridictions to iron thesis have been presented by it's inventer himself. How many contridictions constitute a case of the thesis having failed? How does one know if the iron thesis is a failure, what info do we need and what would it have to look like to accept it as the final nail in the thesis coffin? >Subject: Re: Iron / infection >From: markd@toad-net.com [quoted text clipped - 6 lines] >we need and what would it have to look like to accept it as the final nail >in the thesis coffin? The SHEER NUMBER of researchers investigating the implications of iron .. rules out .. YOU .. in .. the hypothesis .. As if YOU .. are going to go it .. alone .. ? Heh .. heh ... Nature. 2004 Nov 7 [Epub ahead of print] Links Lipocalin 2 mediates an innate immune response to bacterial infection by sequestrating iron. Flo TH, Smith KD, Sato S, Rodriguez DJ, Holmes MA, Strong RK, Akira S, Aderem A. [1] Institute for Systems Biology, Seattle, Washington 98103, USA [2] Institute for Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, 7489 Trondheim, Norway [3] These authors contributed equally to this work. Although iron is required to sustain life, its free concentration and metabolism have to be tightly regulated. This is achieved through a variety of iron-binding proteins including transferrin and ferritin. During infection, bacteria acquire much of their iron from the host by synthesizing siderophores that scavenge iron and transport it into the pathogen. We recently demonstrated that enterochelin, a bacterial catecholate siderophore, binds to the host protein lipocalin 2 (ref. 5). Here, we show that this event is pivotal in the innate immune response to bacterial infection. Upon encountering invading bacteria the Toll-like receptors on immune cells stimulate the transcription, translation and secretion of lipocalin 2; secreted lipocalin 2 then limits bacterial growth by sequestrating the iron-laden siderophore. Our finding represents a new component of the innate immune system and the acute phase response to infection. PMID: 15531878 [PubMed - as supplied by publisher] -------------------------------------------------------------------------- ------ Who loves ya. Tom SignatureJesus Was A Vegetarian! http://jesuswasavegetarian.7h.com Man Is A Herbivore! http://pages.ivillage.com/ironjustice/manisaherbivore DEAD PEOPLE WALKING http://pages.ivillage.com/ironjustice/deadpeoplewalking "The SHEER NUMBER of researchers investigating the implications of iron .. rules out .. YOU .. in .. the hypothesis .." This has always been clear, a confusion that because others are looking at all aspects of biochem in humans that any mention of iron is a mark of some support for your invented thesis,ie. that iron is the cause for all disease. At best this is a confusion about how science works, at worst, well ... There is no where in all the reams of articles you have posted is there even the mere wisper that anyone, anyone in the whole worlds knows about or cares about your invented thesis about iron. If you think this is in error, submit it for publication, or just maybe you have and the results will never be disclosed? You avoid the question, how many articles to the contrary and how many instances of you posting yourself contridictions to your own thesis will constitute clear basis for rejecting it? This is not an empty question, it is at the heart of how science is done, and you should be prepared to answerit. |
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