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10.1371/journal.pone.0136947 http://scihub22266oqcxt.onion/10.1371/journal.pone.0136947 C4552673!4552673 !26317438     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26317438 &cmd=llinks): Failed to open stream: HTTP request failed! 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Roles of TLR/MyD88/MAPK/NF-?B Signaling Pathways in the Regulation of Phagocytosis and Proinflammatory Cytokine Expression in Response to E faecalis Infection |pdf=|usr=}}{{26317438 }} gab.com Text Roles of TLR/MyD88/MAPK/NF- B Signaling Pathways in the Regulation of Phagocytosis and Proinflammatory Cytokine Expression in Response to E faecalis Infection JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26317438 #FOAvip Enterococcus faecalis is a commensal bacterium residing in the gastrointestinal tract of mammals, but in certain situations it is also an opportunistic pathogen which can cause serious disease. Macrophages have been shown to play a critical role in controlling infections by commensal enterococci and also have an important role in mediating chromosomal instability and promoting colon cancer during high-level enterococcal colonization in genetically susceptible mice. However, the molecular mechanisms involved in the interaction of macrophages with enterococci during infection are not fully understood. In this study, using BMDM and RAW264.7 macrophages we show that enterococcal infection activates ERK, JNK and p38 MAPK as well as NF-?B, and drives polarization of macrophages towards the M1 phenotype. Inhibition of NF-?B activation significantly reduced the expression of TNF-? and IL-1?, as did the inhibition of ERK, JNK and p38 MAPK, although to differing extent. Enterococci-induced activation of these pathways and subsequent cytokine expression was contact dependent, modest compared to activation by E. coli and, required the adaptor protein MyD88. Phagocytosis of enterococci by macrophages was enhanced by preopsonization with E. faecalis antiserum and involved the ERK and JNK signaling pathways, with the adaptor protein MyD88 as an important mediator. This study of the interaction of macrophages with enterococci could provide a foundation for studying the pathogenesis of infection by this opportunistic pathogen and to developing new therapeutic approaches to combat enterococcal infection. Twit Text FOAVip Roles of TLR/MyD88/MAPK/NF- B Signaling Pathways in the Regulation of Phagocytosis and Proinflammatory Cytokine Expression in Response to E faecalis Infection ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26317438 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26317438 #FOAvip English Wikipedia <ref>{{Cite pmid|26317438 }}</ref> Roles of TLR/MyD88/MAPK/NF-?B Signaling Pathways in the Regulation of Phagocytosis and Proinflammatory Cytokine Expression in Response to E faecalis Infection #MMPMID26317438 Zou J ; Shankar N PLoS One 2015[]; 10 (8 ): e0136947 PMID26317438 show ga Enterococcus faecalis is a commensal bacterium residing in the gastrointestinal tract of mammals, but in certain situations it is also an opportunistic pathogen which can cause serious disease. Macrophages have been shown to play a critical role in controlling infections by commensal enterococci and also have an important role in mediating chromosomal instability and promoting colon cancer during high-level enterococcal colonization in genetically susceptible mice. However, the molecular mechanisms involved in the interaction of macrophages with enterococci during infection are not fully understood. In this study, using BMDM and RAW264.7 macrophages we show that enterococcal infection activates ERK, JNK and p38 MAPK as well as NF-?B, and drives polarization of macrophages towards the M1 phenotype. Inhibition of NF-?B activation significantly reduced the expression of TNF-? and IL-1?, as did the inhibition of ERK, JNK and p38 MAPK, although to differing extent. Enterococci-induced activation of these pathways and subsequent cytokine expression was contact dependent, modest compared to activation by E. coli and, required the adaptor protein MyD88. Phagocytosis of enterococci by macrophages was enhanced by preopsonization with E. faecalis antiserum and involved the ERK and JNK signaling pathways, with the adaptor protein MyD88 as an important mediator. This study of the interaction of macrophages with enterococci could provide a foundation for studying the pathogenesis of infection by this opportunistic pathogen and to developing new therapeutic approaches to combat enterococcal infection. |Animals [MESH] |Cell Line [MESH] |Cytokines/genetics/*metabolism [MESH] |Disease Models, Animal [MESH] |Enterococcus faecalis/immunology/isolation & purification/*pathogenicity [MESH] |Gram-Positive Bacterial Infections/genetics/*immunology/metabolism/microbiology [MESH] |MAP Kinase Signaling System [MESH] |Macrophages/immunology/microbiology/*physiology [MESH] |Mice [MESH] |Myeloid Differentiation Factor 88/*metabolism [MESH] |NF-kappa B/metabolism [MESH]Roles of TLR/MyD88/MAPK/NF-?B Signaling Pathways in the Regulation of (epmc).pdf DeepDyve Pubget Overpricing