{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"submitter":["Pasmay AA"],"funding":["NIAAA NIH HHS","NIGMS NIH HHS"],"pubmed_abstract":["Adverse in-utero conditions may exert a lifelong impact on neuroimmune function. Our prior work showed that prenatal alcohol exposure (PAE) increases pathological pain sensitivity (allodynia) following peripheral sciatic nerve injury. While the immune mechanism(s) of PAE-induced immune dysfunction are poorly understood, prior studies implicated the involvement of Toll-like receptor 4 (TLR4) and the nucleotide-binding domain, leucine-rich repeat-containing family, pyrin domain-containing 3 (NLRP3) inflammasomes. Interestingly, emerging data suggest a surprising overlap of spinal glial proinflammatory activation via the TLR4-NLRP3-interleukin (IL)-1β axis due to opioid treatment in nerve-injured non-PAE rodents. Considering this preclinical evidence, we explored whether PAE poses a risk fact"],"journal":["bioRxiv : the preprint server for biology"],"pagination":["2025.05.30.655639"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12154580"],"repository":["biostudies-literature"],"pubmed_title":["Prenatal alcohol exposure promotes nerve injury-induced pathological pain following morphine treatment via NLRP3-mediated peripheral and central proinflammatory immune actions."],"pmcid":["PMC12154580"],"funding_grant_id":["T34 GM145428","P20 GM121176","P50 AA022534","R01 AA025967","R01 AA029694"],"pubmed_authors":["Pasmay AA","Carter J","Murphy M","Pritha AN","Fernandez-Oropeza AK","Jones A","Jimenez DC","Noor S","Sun MS","Valenzuela CF"],"additional_accession":[]},"is_claimable":false,"name":"Prenatal alcohol exposure promotes nerve injury-induced pathological pain following morphine treatment via NLRP3-mediated peripheral and central proinflammatory immune actions.","description":"Adverse in-utero conditions may exert a lifelong impact on neuroimmune function. Our prior work showed that prenatal alcohol exposure (PAE) increases pathological pain sensitivity (allodynia) following peripheral sciatic nerve injury. While the immune mechanism(s) of PAE-induced immune dysfunction are poorly understood, prior studies implicated the involvement of Toll-like receptor 4 (TLR4) and the nucleotide-binding domain, leucine-rich repeat-containing family, pyrin domain-containing 3 (NLRP3) inflammasomes. Interestingly, emerging data suggest a surprising overlap of spinal glial proinflammatory activation via the TLR4-NLRP3-interleukin (IL)-1β axis due to opioid treatment in nerve-injured non-PAE rodents. Considering this preclinical evidence, we explored whether PAE poses a risk fact","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 May","modification":"2026-06-03T03:13:25.843Z","creation":"2026-06-03T03:10:38.812Z"},"accession":"S-EPMC12154580","cross_references":{"pubmed":["40501832"],"doi":["10.1101/2025.05.30.655639"]}}