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10.1016/j.pain.2009.09.032 http://scihub22266oqcxt.onion/10.1016/j.pain.2009.09.032 C5515229!5515229!19853379     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=19853379&cmd=llinks): Failed to open stream: HTTP request failed! 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The NALP1 inflammasome controls cytokine production and nociception in a rat fracture model of complex regional pain syndrome |pdf=|usr=}}{{19853379}} gab.com Text The NALP1 inflammasome controls cytokine production and nociception in a rat fracture model of complex regional pain syndrome JO: Pain http://www.kidney.de/pget.php?&tw=1&pmid=19853379 #FOAvip Tibia fracture followed by limb immobilization in rats evokes nociceptive and vascular changes resembling complex regional pain syndrome type I (CRPS I). Previously we observed that substance P (SP) and interleukin-1? (IL-1?) signaling contribute to chronic regional nociceptive sensitization in this model. It is known that inflammasome multiprotein complexes containing caspase-1 and NALP1 are involved in the activation of the IL-1? family of pro-nociceptive cytokines expressed in skin and other tissues. Therefore, we hypothesized that SP activated inflammasomes might contribute to mechanical allodynia after fracture. Using this model we observed that: 1) inflammasome components and products NALP1, caspase-1, IL-1? and IL-18 were present in low levels in normal skin, but expression of all these was strongly up-regulated after fracture, 2) NALP1, caspase-1 and IL-1? were co-expressed in keratinocytes, and the number of NALP1, caspase-1, and IL-1? positive cells dramatically increased at 4 weeks post-fracture, 3) LY303870, an NK1 receptor antagonist, effectively blocked fracture induced up-regulation of activated inflammasome components and cytokines, 4) IL-1? and IL-18 intraplantar injection induced mechanical allodynia in normal rats, and 5) both a selective caspase-1 inhibitor and an IL-1 receptor antagonist attenuated fracture induced hind paw mechanical allodynia. Collectively, these data suggest that NALP1 containing inflammasomes activated by NK1 receptors are expressed in keratinocytes and contribute to post-traumatic regional nociceptive sensitization. These findings highlight the possible importance of neuro-cutaneous signaling and innate immunity mechanisms in the development of CRPS. Twit Text FOAVip The NALP1 inflammasome controls cytokine production and nociception in a rat fracture model of complex regional pain syndrome ????Pain http://www.kidney.de/pget.php?&tw=1&pmid=19853379 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=19853379 #FOAvip English Wikipedia <ref>{{Cite pmid|19853379}}</ref> The NALP1 inflammasome controls cytokine production and nociception in a rat fracture model of complex regional pain syndrome #MMPMID19853379 Li WW; Guo TZ; Liang D; Shi X; Wei T; Kingery WS; Clark JD Pain 2009[Dec]; 147 (1-3): 277-86 PMID19853379show ga Tibia fracture followed by limb immobilization in rats evokes nociceptive and vascular changes resembling complex regional pain syndrome type I (CRPS I). Previously we observed that substance P (SP) and interleukin-1? (IL-1?) signaling contribute to chronic regional nociceptive sensitization in this model. It is known that inflammasome multiprotein complexes containing caspase-1 and NALP1 are involved in the activation of the IL-1? family of pro-nociceptive cytokines expressed in skin and other tissues. Therefore, we hypothesized that SP activated inflammasomes might contribute to mechanical allodynia after fracture. Using this model we observed that: 1) inflammasome components and products NALP1, caspase-1, IL-1? and IL-18 were present in low levels in normal skin, but expression of all these was strongly up-regulated after fracture, 2) NALP1, caspase-1 and IL-1? were co-expressed in keratinocytes, and the number of NALP1, caspase-1, and IL-1? positive cells dramatically increased at 4 weeks post-fracture, 3) LY303870, an NK1 receptor antagonist, effectively blocked fracture induced up-regulation of activated inflammasome components and cytokines, 4) IL-1? and IL-18 intraplantar injection induced mechanical allodynia in normal rats, and 5) both a selective caspase-1 inhibitor and an IL-1 receptor antagonist attenuated fracture induced hind paw mechanical allodynia. Collectively, these data suggest that NALP1 containing inflammasomes activated by NK1 receptors are expressed in keratinocytes and contribute to post-traumatic regional nociceptive sensitization. These findings highlight the possible importance of neuro-cutaneous signaling and innate immunity mechanisms in the development of CRPS. äThe NALP1 inflammasome controls cytokine production and nociception in(epmc).pdf DeepDyve Pubget Overpricing