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10.1007/s00281-016-0581-1 http://scihub22266oqcxt.onion/10.1007/s00281-016-0581-1 C5233600!5233600!27405866     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Semin+Immunopathol 2017 ; 39 (2): 215-23 Nephropedia Template TP {{tp|p=27405866|t=2017. The role of NLRP3 and AIM2 in inflammasome activation during Brucella abortus infection |pdf=|usr=}}{{27405866}} gab.com Text The role of NLRP3 and AIM2 in inflammasome activation during Brucella abortus infection JO: Semin Immunopathol http://www.kidney.de/pget.php?&tw=1&pmid=27405866 #FOAvip The innate immune system is essential for detection and elimination of bacterial pathogens. Upon inflammasome activation, caspase-1 cleaves pro-IL-1? and pro-IL-18 to their mature forms IL-1? and IL-18, respectively, and the cell undergoes inflammatory death termed pyroptosis. Here we reviewed recent findings demonstrating that Brucella abortus ligands activate NLRP3 and AIM2 inflammasomes which leads to control of infection. This protective effect is due to inflammatory response caused by IL-1? and IL-18 rather than cell death. Brucella DNA is sensed by AIM2 and bacteria induced mitochondrial reactive oxygen species is detected by NLRP3. However, deregulation of proinflammatory cytokine production can lead to immunopathology. Nervous system invasion by bacteria of the genus Brucella results in an inflammatory disorder termed neurobrucellosis. Herein we discuss the mechanism of caspase-1 activation and IL-1? secretion in glial cells infected with B. abortus. Our results demonstrate that the ASC inflammasome is indispensable for inducing the activation of caspase-1 and secretion of IL-1? upon infection of astrocytes and microglia with Brucella. Moreover, our results demonstrate that secretion of IL-1? by Brucella-infected glial cells depends on NLRP3 and AIM2 and leads to neurobrucellosis. Further, the inhibition of the host cell inflammasome as an immune evasion strategy has been described for bacterial pathogens. We discuss here that the bacterial type IV secretion system VirB is required for inflammasome activation in host cells during infection. Taken together, our results indicate that Brucella is sensed by ASC inflammasomes mainly NLRP3 and AIM2 that collectively orchestrate a robust caspase-1 activation and proinflammatory response. Twit Text FOAVip The role of NLRP3 and AIM2 in inflammasome activation during Brucella abortus infection ????Semin Immunopathol http://www.kidney.de/pget.php?&tw=1&pmid=27405866 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27405866 #FOAvip English Wikipedia <ref>{{Cite pmid|27405866}}</ref> The role of NLRP3 and AIM2 in inflammasome activation during Brucella abortus infection #MMPMID27405866 Marim FM; Franco MMC; Gomes MTR; Miraglia MC; Giambartolomei GH; Oliveira SC Semin Immunopathol 2017[Feb]; 39 (2): 215-23 PMID27405866show ga The innate immune system is essential for detection and elimination of bacterial pathogens. Upon inflammasome activation, caspase-1 cleaves pro-IL-1? and pro-IL-18 to their mature forms IL-1? and IL-18, respectively, and the cell undergoes inflammatory death termed pyroptosis. Here we reviewed recent findings demonstrating that Brucella abortus ligands activate NLRP3 and AIM2 inflammasomes which leads to control of infection. This protective effect is due to inflammatory response caused by IL-1? and IL-18 rather than cell death. Brucella DNA is sensed by AIM2 and bacteria induced mitochondrial reactive oxygen species is detected by NLRP3. However, deregulation of proinflammatory cytokine production can lead to immunopathology. Nervous system invasion by bacteria of the genus Brucella results in an inflammatory disorder termed neurobrucellosis. Herein we discuss the mechanism of caspase-1 activation and IL-1? secretion in glial cells infected with B. abortus. Our results demonstrate that the ASC inflammasome is indispensable for inducing the activation of caspase-1 and secretion of IL-1? upon infection of astrocytes and microglia with Brucella. Moreover, our results demonstrate that secretion of IL-1? by Brucella-infected glial cells depends on NLRP3 and AIM2 and leads to neurobrucellosis. Further, the inhibition of the host cell inflammasome as an immune evasion strategy has been described for bacterial pathogens. We discuss here that the bacterial type IV secretion system VirB is required for inflammasome activation in host cells during infection. Taken together, our results indicate that Brucella is sensed by ASC inflammasomes mainly NLRP3 and AIM2 that collectively orchestrate a robust caspase-1 activation and proinflammatory response. äThe role of NLRP3 and AIM2 in inflammasome activation during Brucella (epmc).pdf DeepDyve Pubget Overpricing