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10.1128/IAI.00144-15 http://scihub22266oqcxt.onion/10.1128/IAI.00144-15 C4534669!4534669 !26099585     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 284.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 284.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26099585 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Infect+Immun 2015 ; 83 (9 ): 3534-44 Nephropedia Template TP {{tp|p=26099585 |t=2015. Lack of the Transcription Factor Hypoxia-Inducible Factor 1? (HIF-1?) in Macrophages Accelerates the Necrosis of Mycobacterium avium-Induced Granulomas |pdf=|usr=}}{{26099585 }} gab.com Text Lack of the Transcription Factor Hypoxia-Inducible Factor 1 (HIF-1 ) in Macrophages Accelerates the Necrosis of Mycobacterium avium-Induced Granulomas JO: Infect Immun http://www.kidney.de/pget.php?&tw=1&pmid=26099585 #FOAvip The establishment of mycobacterial infection is characterized by the formation of granulomas, which are well-organized aggregates of immune cells, namely, infected macrophages. The granuloma's main function is to constrain and prevent dissemination of the mycobacteria while focusing the immune response to a limited area. In some cases these lesions can grow progressively into large granulomas which can undergo central necrosis, thereby leading to their caseation. Macrophages are the most abundant cells present in the granuloma and are known to adapt under hypoxic conditions in order to avoid cell death. Our laboratory has developed a granuloma necrosis model that mimics the human pathology of Mycobacterium tuberculosis, using C57BL/6 mice infected intravenously with a low dose of a highly virulent strain of Mycobacterium avium. In this work, a mouse strain deleted of the hypoxia inducible factor 1? (HIF-1?) under the Cre-lox system regulated by the lysozyme M gene promoter was used to determine the relevance of HIF-1? in the caseation of granulomas. The genetic ablation of HIF-1? in the myeloid lineage causes the earlier emergence of granuloma necrosis and clearly induces an impairment of the resistance against M. avium infection coincident with the emergence of necrosis. The data provide evidence that granulomas become hypoxic before undergoing necrosis through the analysis of vascularization and quantification of HIF-1? in a necrotizing mouse model. Our results show that interfering with macrophage adaptation to hypoxia, such as through HIF-1? inactivation, accelerates granuloma necrosis. Twit Text FOAVip Lack of the Transcription Factor Hypoxia-Inducible Factor 1 (HIF-1 ) in Macrophages Accelerates the Necrosis of Mycobacterium avium-Induced Granulomas ????Infect Immun http://www.kidney.de/pget.php?&tw=1&pmid=26099585 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26099585 #FOAvip English Wikipedia <ref>{{Cite pmid|26099585 }}</ref> Lack of the Transcription Factor Hypoxia-Inducible Factor 1? (HIF-1?) in Macrophages Accelerates the Necrosis of Mycobacterium avium-Induced Granulomas #MMPMID26099585 Cardoso MS ; Silva TM ; Resende M ; Appelberg R ; Borges M Infect Immun 2015[Sep]; 83 (9 ): 3534-44 PMID26099585 show ga The establishment of mycobacterial infection is characterized by the formation of granulomas, which are well-organized aggregates of immune cells, namely, infected macrophages. The granuloma's main function is to constrain and prevent dissemination of the mycobacteria while focusing the immune response to a limited area. In some cases these lesions can grow progressively into large granulomas which can undergo central necrosis, thereby leading to their caseation. Macrophages are the most abundant cells present in the granuloma and are known to adapt under hypoxic conditions in order to avoid cell death. Our laboratory has developed a granuloma necrosis model that mimics the human pathology of Mycobacterium tuberculosis, using C57BL/6 mice infected intravenously with a low dose of a highly virulent strain of Mycobacterium avium. In this work, a mouse strain deleted of the hypoxia inducible factor 1? (HIF-1?) under the Cre-lox system regulated by the lysozyme M gene promoter was used to determine the relevance of HIF-1? in the caseation of granulomas. The genetic ablation of HIF-1? in the myeloid lineage causes the earlier emergence of granuloma necrosis and clearly induces an impairment of the resistance against M. avium infection coincident with the emergence of necrosis. The data provide evidence that granulomas become hypoxic before undergoing necrosis through the analysis of vascularization and quantification of HIF-1? in a necrotizing mouse model. Our results show that interfering with macrophage adaptation to hypoxia, such as through HIF-1? inactivation, accelerates granuloma necrosis. |Animals [MESH] |Disease Models, Animal [MESH] |Flow Cytometry [MESH] |Granuloma/*pathology [MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/*metabolism [MESH] |Immunohistochemistry [MESH] |In Situ Nick-End Labeling [MESH] |Macrophages/*metabolism [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Mycobacterium Infections/metabolism/*pathology [MESH] |Mycobacterium avium [MESH]Lack of the Transcription Factor Hypoxia-Inducible Factor 1? (HIF-1?) (epmc).pdf DeepDyve Pubget Overpricing