Matches in DBpedia 2016-04 for { <http://doi.org/10.1038/ncomms2023> ?p ?o }
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- ncomms2023 doi "10.1038/ncomms2023".
- ncomms2023 isCitedBy Damage-associated_molecular_pattern.
- ncomms2023 journal "Nat Commun".
- ncomms2023 pages "1034".
- ncomms2023 pmc "3658010".
- ncomms2023 pmid "22948816".
- ncomms2023 quote "Here, we showed that colitis aggravated by P2X7-mediated activation of MCs was independent of the inflammasome pathway, and that P2X7-mediated activation of MCs promoted TNFα production by effector cells to further promote intestinal inflammation44. Our findings also suggest that MCs exacerbate inflammation by recruiting neutrophils to produce abundant TNFα, but less IL-10 than is produced by other cells . This neutrophil recruitment was mediated by the production of IL-1β, LTs and chemokines, which are potential targets for the treatment of colitis. Mice with experimentally induced colitis that lack CXCR2 or 5-LO , as well as mice treated with inhibitors of CCR2, CXCR2 or 5-LO, show reduced inflammation and less neutrophil recruitment in their colons33,45,46. Moreover, given that ATP promotes neutrophil migration47, it is possible that P2X7-dependent LT and chemokine production, as well as ATP generation via AK2 and ATP synthase from MCs, could amplify neutrophil infiltration of the colon. These data collectively indicate that MCs are key factors in the induction of intestinal inflammation and also recruit neutrophils to heighten inflammatory responses. P2X7-dependent MC activation could, therefore, be a target for the treatment of intestinal inflammation.".
- ncomms2023 title "Extracellular ATP mediates mast cell-dependent intestinal inflammation through P2X7 purinoceptors".
- ncomms2023 vauthors "Kurashima Y, Amiya T, Nochi T, et al.".
- ncomms2023 volume "3".
- ncomms2023 year "2012".