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Prenatal alcohol exposure promotes NLRP3 inflammasome-dependent immune actions following morphine treatment and paradoxically prolongs nerve injury-induced pathological pain in female mice.
Authors
Noor S, Sun MS, Pasmay AA, Pritha AN, Ruffaner-Hanson CD, Nysus MV, Jimenez DC, Murphy M, Savage DD, Valenzuela CF, Milligan EDAbstract
Neuroimmune dysregulation from prenatal alcohol exposure (PAE) may contribute to neurological deficits associated with fetal alcohol spectrum disorders (FASD). PAE is a risk factor for developing peripheral immune and spinal glial sensitization and release of the proinflammatory cytokine IL-1β, which lead to neuropathic pain (allodynia) from minor nerve injury. Although morphine acts on μ-opioid receptors, it also activates immune receptors, TLR4, and the NLRP3 inflammasome that induces IL-1β. We hypothesized that PAE induces NLRP3 sensitization by morphine following nerve injury in adult mice.