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10.1038/srep15214 http://scihub22266oqcxt.onion/10.1038/srep15214 C4606593!4606593 !26469538     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26469538 &cmd=llinks): Failed to open stream: HTTP request failed! 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Expression profiling of lymph nodes in tuberculosis patients reveal inflammatory milieu at site of infection |pdf=|usr=}}{{26469538 }} gab.com Text Expression profiling of lymph nodes in tuberculosis patients reveal inflammatory milieu at site of infection JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26469538 #FOAvip Extrapulmonary manifestations constitute 15 to 20% of tuberculosis cases, with lymph node tuberculosis (LNTB) as the most common form of infection. However, diagnosis and treatment advances are hindered by lack of understanding of LNTB biology. To identify host response, Mycobacterium tuberculosis infected lymph nodes from LNTB patients were studied by means of transcriptomics and quantitative proteomics analyses. The selected targets obtained by comparative analyses were validated by quantitative PCR and immunohistochemistry. This approach provided expression data for 8,728 transcripts and 102 proteins, differentially regulated in the infected human lymph node. Enhanced inflammation with upregulation of T-helper1-related genes, combined with marked dysregulation of matrix metalloproteinases, indicates tissue damage due to high immunoactivity at infected niche. This expression signature was accompanied by significant upregulation of an immunoregulatory gene, leukotriene A4 hydrolase, at both transcript and protein levels. Comparative transcriptional analyses revealed LNTB-specific perturbations. In contrast to pulmonary TB-associated increase in lipid metabolism, genes involved in fatty-acid metabolism were found to be downregulated in LNTB suggesting differential lipid metabolic signature. This study investigates the tissue molecular signature of LNTB patients for the first time and presents findings that indicate the possible mechanism of disease pathology through dysregulation of inflammatory and tissue-repair processes. Twit Text FOAVip Expression profiling of lymph nodes in tuberculosis patients reveal inflammatory milieu at site of infection ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26469538 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26469538 #FOAvip English Wikipedia <ref>{{Cite pmid|26469538 }}</ref> Expression profiling of lymph nodes in tuberculosis patients reveal inflammatory milieu at site of infection #MMPMID26469538 Maji A ; Misra R ; Kumar Mondal A ; Kumar D ; Bajaj D ; Singhal A ; Arora G ; Bhaduri A ; Sajid A ; Bhatia S ; Singh S ; Singh H ; Rao V ; Dash D ; Baby Shalini E ; Sarojini Michael J ; Chaudhary A ; Gokhale RS ; Singh Y Sci Rep 2015[Oct]; 5 (ä): 15214 PMID26469538 show ga Extrapulmonary manifestations constitute 15 to 20% of tuberculosis cases, with lymph node tuberculosis (LNTB) as the most common form of infection. However, diagnosis and treatment advances are hindered by lack of understanding of LNTB biology. To identify host response, Mycobacterium tuberculosis infected lymph nodes from LNTB patients were studied by means of transcriptomics and quantitative proteomics analyses. The selected targets obtained by comparative analyses were validated by quantitative PCR and immunohistochemistry. This approach provided expression data for 8,728 transcripts and 102 proteins, differentially regulated in the infected human lymph node. Enhanced inflammation with upregulation of T-helper1-related genes, combined with marked dysregulation of matrix metalloproteinases, indicates tissue damage due to high immunoactivity at infected niche. This expression signature was accompanied by significant upregulation of an immunoregulatory gene, leukotriene A4 hydrolase, at both transcript and protein levels. Comparative transcriptional analyses revealed LNTB-specific perturbations. In contrast to pulmonary TB-associated increase in lipid metabolism, genes involved in fatty-acid metabolism were found to be downregulated in LNTB suggesting differential lipid metabolic signature. This study investigates the tissue molecular signature of LNTB patients for the first time and presents findings that indicate the possible mechanism of disease pathology through dysregulation of inflammatory and tissue-repair processes. |*Gene Expression Profiling [MESH] |Adolescent [MESH] |Adult [MESH] |Child [MESH] |Cytokines/genetics/metabolism [MESH] |Epoxide Hydrolases/genetics/metabolism [MESH] |Fatty Acids/metabolism [MESH] |Female [MESH] |Humans [MESH] |Immunohistochemistry [MESH] |Lipid Metabolism/genetics [MESH] |Lymph Nodes/*metabolism [MESH] |Male [MESH] |Matrix Metalloproteinases/genetics/metabolism [MESH] |Proteomics [MESH] |Real-Time Polymerase Chain Reaction [MESH] |Th1 Cells/immunology/metabolism [MESH] |Th2 Cells/immunology/metabolism [MESH] |Transcriptome [MESH]Expression profiling of lymph nodes in tuberculosis patients reveal in(epmc).pdf DeepDyve Pubget Overpricing