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10.1152/ajplung.00075.2017 http://scihub22266oqcxt.onion/10.1152/ajplung.00075.2017 C5538876!5538876 !28408365     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28408365 &cmd=llinks): Failed to open stream: HTTP request failed! 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Immunomodulators targeting MARCO expression improve resistance to postinfluenza bacterial pneumonia |pdf=|usr=}}{{28408365 }} gab.com Text Immunomodulators targeting MARCO expression improve resistance to postinfluenza bacterial pneumonia JO: Am J Physiol Lung Cell Mol Physiol http://www.kidney.de/pget.php?&tw=1&pmid=28408365 #FOAvip Downregulation of the alveolar macrophage (AM) receptor with collagenous structure (MARCO) leads to susceptibility to postinfluenza bacterial pneumonia, a major cause of morbidity and mortality. We sought to determine whether immunomodulation of MARCO could improve host defense and resistance to secondary bacterial pneumonia. RNAseq analysis identified a striking increase in MARCO expression between days 9 and 11 after influenza infection and indicated important roles for Akt and Nrf2 in MARCO recovery. In vitro, primary human AM-like monocyte-derived macrophages (AM-MDMs) and THP-1 macrophages were treated with IFN? to model influenza effects. Activators of Nrf2 (sulforaphane) or Akt (SC79) caused increased MARCO expression and a MARCO-dependent improvement in phagocytosis in IFN?-treated cells and improved survival in mice with postinfluenza pneumococcal pneumonia. Transcription factor analysis also indicated a role for transcription factor E-box (TFEB) in MARCO recovery. Overexpression of TFEB in THP-1 cells led to marked increases in MARCO. The ability of Akt activation to increase MARCO expression in IFN?-treated AM-MDMs was abrogated in TFEB-knockdown cells, indicating Akt increases MARCO expression through TFEB. Increasing MARCO expression by targeting Nrf2 signaling or the Akt-TFEB-MARCO pathway are promising strategies to improve bacterial clearance and survival in postinfluenza bacterial pneumonia. Twit Text FOAVip Immunomodulators targeting MARCO expression improve resistance to postinfluenza bacterial pneumonia ????Am J Physiol Lung Cell Mol Physiol http://www.kidney.de/pget.php?&tw=1&pmid=28408365 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28408365 #FOAvip English Wikipedia <ref>{{Cite pmid|28408365 }}</ref> Immunomodulators targeting MARCO expression improve resistance to postinfluenza bacterial pneumonia #MMPMID28408365 Wu M ; Gibbons JG ; DeLoid GM ; Bedugnis AS ; Thimmulappa RK ; Biswal S ; Kobzik L Am J Physiol Lung Cell Mol Physiol 2017[Jul]; 313 (1 ): L138-L153 PMID28408365 show ga Downregulation of the alveolar macrophage (AM) receptor with collagenous structure (MARCO) leads to susceptibility to postinfluenza bacterial pneumonia, a major cause of morbidity and mortality. We sought to determine whether immunomodulation of MARCO could improve host defense and resistance to secondary bacterial pneumonia. RNAseq analysis identified a striking increase in MARCO expression between days 9 and 11 after influenza infection and indicated important roles for Akt and Nrf2 in MARCO recovery. In vitro, primary human AM-like monocyte-derived macrophages (AM-MDMs) and THP-1 macrophages were treated with IFN? to model influenza effects. Activators of Nrf2 (sulforaphane) or Akt (SC79) caused increased MARCO expression and a MARCO-dependent improvement in phagocytosis in IFN?-treated cells and improved survival in mice with postinfluenza pneumococcal pneumonia. Transcription factor analysis also indicated a role for transcription factor E-box (TFEB) in MARCO recovery. Overexpression of TFEB in THP-1 cells led to marked increases in MARCO. The ability of Akt activation to increase MARCO expression in IFN?-treated AM-MDMs was abrogated in TFEB-knockdown cells, indicating Akt increases MARCO expression through TFEB. Increasing MARCO expression by targeting Nrf2 signaling or the Akt-TFEB-MARCO pathway are promising strategies to improve bacterial clearance and survival in postinfluenza bacterial pneumonia. |*Disease Resistance [MESH] |Animals [MESH] |Base Sequence [MESH] |Basic Helix-Loop-Helix Leucine Zipper Transcription Factors [MESH] |Bronchoalveolar Lavage Fluid [MESH] |Catechin/analogs & derivatives/pharmacology [MESH] |Cell Line [MESH] |Cytokines/metabolism [MESH] |Host-Pathogen Interactions/immunology [MESH] |Humans [MESH] |Immunologic Factors/*pharmacology [MESH] |Influenza, Human/*complications [MESH] |Interferon-gamma/pharmacology [MESH] |Isothiocyanates/pharmacology [MESH] |MAP Kinase Kinase Kinases/metabolism [MESH] |Macrophages, Alveolar/metabolism [MESH] |Male [MESH] |Mice, Inbred C57BL [MESH] |Models, Biological [MESH] |Orthomyxoviridae Infections/complications [MESH] |Phagocytosis/drug effects [MESH] |Pneumonia, Bacterial/*etiology/*immunology [MESH] |Promoter Regions, Genetic/genetics [MESH] |Proto-Oncogene Proteins c-akt/metabolism [MESH] |RNA, Messenger/genetics/metabolism [MESH] |Receptors, Immunologic/genetics/*metabolism [MESH] |Sequence Analysis, RNA [MESH] |Signal Transduction [MESH] |Staphylococcus aureus/drug effects [MESH] |Sulfoxides [MESH]Immunomodulators targeting MARCO expression improve resistance to post(epmc).pdf DeepDyve Pubget Overpricing