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10.1016/j.jneuroim.2021.577654 http://scihub22266oqcxt.onion/10.1016/j.jneuroim.2021.577654 34265624!8243641!34265624     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=34265624&cmd=llinks): Failed to open stream: HTTP request failed! 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N-acylethanolamine regulation of TLR3-induced hyperthermia and neuroinflammatory gene expression: A role for PPARalpha |pdf=|usr=}}{{34265624}} gab.com Text N-acylethanolamine regulation of TLR3-induced hyperthermia and neuroinflammatory gene expression: A role for PPARalpha JO: J Neuroimmunol http://www.kidney.de/pget.php?&tw=1&pmid=34265624 #FOAvip Increasing evidence suggests that SARS-CoV-2, the virus responsible for the COVID-19 pandemic, is associated with increased risk of developing neurological or psychiatric conditions such as depression, anxiety or dementia. While the precise mechanism underlying this association is unknown, aberrant activation of toll-like receptor (TLR)3, a viral recognizing pattern recognition receptor, may play a key role. Synthetic cannabinoids and enhancing cannabinoid tone via inhibition of fatty acid amide hydrolase (FAAH) has been demonstrated to modulate TLR3-induced neuroimmune responses and associated sickness behaviour. However, the role of individual FAAH substrates, and the receptor mechanisms mediating these effects, are unknown. The present study examined the effects of intracerebral or systemic administration of the FAAH substrates N-oleoylethanolamide (OEA), N-palmitoylethanolamide (PEA) or the anandamide (AEA) analogue meth-AEA on hyperthermia and hypothalamic inflammatory gene expression following administration of the TLR3 agonist, and viral mimetic, poly I:C. The data demonstrate that meth-AEA does not alter TLR3-induced hyperthermia or hypothalamic inflammatory gene expression. In comparison, OEA and PEA attenuated the TLR3-induced hyperthermia, although only OEA attenuated the expression of hyperthermia-related genes (IL-1beta, iNOS, COX2 and m-PGES) in the hypothalamus. OEA, but not PEA, attenuated TLR3-induced increases in the expression of all IRF- and NFkappaB-related genes examined in the hypothalamus, but not in the spleen. Antagonism of PPARalpha prevented the OEA-induced attenuation of IRF- and NFkappaB-related genes in the hypothalamus following TLR3 activation but did not significantly alter temperature. PPARalpha agonism did not alter TLR3-induced hyperthermia or hypothalamic inflammatory gene expression. These data indicate that OEA may be the primary FAAH substrate that modulates TLR3-induced neuroinflammation and hyperthermia, effects partially mediated by PPARalpha. Twit Text FOAVip N-acylethanolamine regulation of TLR3-induced hyperthermia and neuroinflammatory gene expression: A role for PPARalpha ????J Neuroimmunol http://www.kidney.de/pget.php?&tw=1&pmid=34265624 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34265624 #FOAvip English Wikipedia <ref>{{Cite pmid|34265624}}</ref> N-acylethanolamine regulation of TLR3-induced hyperthermia and neuroinflammatory gene expression: A role for PPARalpha #MMPMID34265624 Flannery LE; Kerr DM; Hughes EM; Kelly C; Costello J; Thornton AM; Humphrey RM; Finn DP; Roche M J Neuroimmunol 2021[Sep]; 358 (�): 577654 PMID34265624show ga Increasing evidence suggests that SARS-CoV-2, the virus responsible for the COVID-19 pandemic, is associated with increased risk of developing neurological or psychiatric conditions such as depression, anxiety or dementia. While the precise mechanism underlying this association is unknown, aberrant activation of toll-like receptor (TLR)3, a viral recognizing pattern recognition receptor, may play a key role. Synthetic cannabinoids and enhancing cannabinoid tone via inhibition of fatty acid amide hydrolase (FAAH) has been demonstrated to modulate TLR3-induced neuroimmune responses and associated sickness behaviour. However, the role of individual FAAH substrates, and the receptor mechanisms mediating these effects, are unknown. The present study examined the effects of intracerebral or systemic administration of the FAAH substrates N-oleoylethanolamide (OEA), N-palmitoylethanolamide (PEA) or the anandamide (AEA) analogue meth-AEA on hyperthermia and hypothalamic inflammatory gene expression following administration of the TLR3 agonist, and viral mimetic, poly I:C. The data demonstrate that meth-AEA does not alter TLR3-induced hyperthermia or hypothalamic inflammatory gene expression. In comparison, OEA and PEA attenuated the TLR3-induced hyperthermia, although only OEA attenuated the expression of hyperthermia-related genes (IL-1beta, iNOS, COX2 and m-PGES) in the hypothalamus. OEA, but not PEA, attenuated TLR3-induced increases in the expression of all IRF- and NFkappaB-related genes examined in the hypothalamus, but not in the spleen. Antagonism of PPARalpha prevented the OEA-induced attenuation of IRF- and NFkappaB-related genes in the hypothalamus following TLR3 activation but did not significantly alter temperature. PPARalpha agonism did not alter TLR3-induced hyperthermia or hypothalamic inflammatory gene expression. These data indicate that OEA may be the primary FAAH substrate that modulates TLR3-induced neuroinflammation and hyperthermia, effects partially mediated by PPARalpha. |Amidohydrolases/pharmacology[MESH] |Animals[MESH] |Ethanolamines/*pharmacology[MESH] |Female[MESH] |Gene Expression[MESH] |Hyperthermia, Induced/*methods[MESH] |Inflammation Mediators/*metabolism[MESH] |PPAR alpha/agonists/antagonists & inhibitors/*metabolism[MESH] |Poly I-C/toxicity[MESH] |Rats[MESH] |Rats, Sprague-Dawley[MESH]N-acylethanolamine regulation of TLR3-induced hyperthermia and neuroin(epmc).pdf DeepDyve Pubget Overpricing