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Storage lipid studies in tuberculosis reveal that foam cell biogenesis is disease-specific.

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Title: Storage lipid studies in tuberculosis reveal that foam cell biogenesis is disease-specific.
Authors: Guerrini, Valentina1, Prideaux, Brendan1, Blanc, Landry1, Bruiners, Natalie1, Arrigucci, Riccardo1, Singh, Sukhwinder2, Ho-Liang, Hsin Pin1, Salamon, Hugh3, Chen, Pei-Yu1, Lakehal, Karim1, Subbian, Selvakumar1, O'brien, Paul1, Via, Laura E.4, 3rdbarry, Clifton E.4, Dartois, Véronique1, Gennaro, Maria Laura1 marila.gennaro@rutgers.edu
Source: PLoS Pathogens. 8/30/2018, Vol. 14 Issue 8, p1-27. 27p.
Subject Terms: *MACROPHAGES, *INFLAMMATION, *ATHEROSCLEROSIS, *MYCOBACTERIUM tuberculosis, *TUMOR necrosis factor receptors, *IN vitro studies
Abstract: Foam cells are lipid-laden macrophages that contribute to the inflammation and tissue damage associated with many chronic inflammatory disorders. Although foam cell biogenesis has been extensively studied in atherosclerosis, how these cells form during a chronic infectious disease such as tuberculosis is unknown. Here we report that, unlike the cholesterol-laden cells of atherosclerosis, foam cells in tuberculous lung lesions accumulate triglycerides. Consequently, the biogenesis of foam cells varies with the underlying disease. In vitro mechanistic studies showed that triglyceride accumulation in human macrophages infected with Mycobacterium tuberculosis is mediated by TNF receptor signaling through downstream activation of the caspase cascade and the mammalian target of rapamycin complex 1 (mTORC1). These features are distinct from the known biogenesis of atherogenic foam cells and establish a new paradigm for non-atherogenic foam cell formation. Moreover, they reveal novel targets for disease-specific pharmacological interventions against maladaptive macrophage responses. [ABSTRACT FROM AUTHOR]
Copyright of PLoS Pathogens is the property of Public Library of Science and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Storage lipid studies in tuberculosis reveal that foam cell biogenesis is disease-specific.
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  Data: <searchLink fieldCode="AR" term="%22Guerrini%2C+Valentina%22">Guerrini, Valentina</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Prideaux%2C+Brendan%22">Prideaux, Brendan</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Blanc%2C+Landry%22">Blanc, Landry</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Bruiners%2C+Natalie%22">Bruiners, Natalie</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Arrigucci%2C+Riccardo%22">Arrigucci, Riccardo</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Singh%2C+Sukhwinder%22">Singh, Sukhwinder</searchLink><relatesTo>2</relatesTo><br /><searchLink fieldCode="AR" term="%22Ho-Liang%2C+Hsin+Pin%22">Ho-Liang, Hsin Pin</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Salamon%2C+Hugh%22">Salamon, Hugh</searchLink><relatesTo>3</relatesTo><br /><searchLink fieldCode="AR" term="%22Chen%2C+Pei-Yu%22">Chen, Pei-Yu</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Lakehal%2C+Karim%22">Lakehal, Karim</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Subbian%2C+Selvakumar%22">Subbian, Selvakumar</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22O'brien%2C+Paul%22">O'brien, Paul</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Via%2C+Laura+E%2E%22">Via, Laura E.</searchLink><relatesTo>4</relatesTo><br /><searchLink fieldCode="AR" term="%223rdbarry%2C+Clifton+E%2E%22">3rdbarry, Clifton E.</searchLink><relatesTo>4</relatesTo><br /><searchLink fieldCode="AR" term="%22Dartois%2C+Véronique%22">Dartois, Véronique</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Gennaro%2C+Maria+Laura%22">Gennaro, Maria Laura</searchLink><relatesTo>1</relatesTo><i> marila.gennaro@rutgers.edu</i>
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  Data: <searchLink fieldCode="JN" term="%22PLoS+Pathogens%22">PLoS Pathogens</searchLink>. 8/30/2018, Vol. 14 Issue 8, p1-27. 27p.
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  Data: Foam cells are lipid-laden macrophages that contribute to the inflammation and tissue damage associated with many chronic inflammatory disorders. Although foam cell biogenesis has been extensively studied in atherosclerosis, how these cells form during a chronic infectious disease such as tuberculosis is unknown. Here we report that, unlike the cholesterol-laden cells of atherosclerosis, foam cells in tuberculous lung lesions accumulate triglycerides. Consequently, the biogenesis of foam cells varies with the underlying disease. In vitro mechanistic studies showed that triglyceride accumulation in human macrophages infected with Mycobacterium tuberculosis is mediated by TNF receptor signaling through downstream activation of the caspase cascade and the mammalian target of rapamycin complex 1 (mTORC1). These features are distinct from the known biogenesis of atherogenic foam cells and establish a new paradigm for non-atherogenic foam cell formation. Moreover, they reveal novel targets for disease-specific pharmacological interventions against maladaptive macrophage responses. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of PLoS Pathogens is the property of Public Library of Science and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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