This study investigates the role of N-acylethanolamine acid amidase (NAAA) in monocytes and its impact on the development of hyperalgesic priming, a model for pain chronification. The research explores how NAAA activity in monocytes influences lipid signaling pathways, particularly those involving peroxisome proliferator-activated receptor-alpha (PPAR-α), and contributes to the transition from acute to chronic pain states.
Mice lacking Naaa in CD11b+ myeloid cells exhibited resistance to hyperalgesic priming, indicating that NAAA activity in these cells is crucial for the development of pain chronification. Pharmacological inhibition of NAAA also prevented hyperalgesic priming in wild-type mice, an effect that was dependent on PPAR-α signaling.
The study utilized a conditional Knockout mouse model in which the Naaa gene was specifically deleted in CD11b+ myeloid cells (monocytes and macrophages). This was achieved by inserting loxP sites flanking critical exons of the Naaa gene, allowing for tissue-specific deletion upon expression of Cre recombinase under the CD11b promoter.
Pain chronification, Hyperalgesic priming, Monocyte function, Lipid signaling, NAAA, PPAR-α
Conditional Knockout, Myeloid cell-specific deletion, Cre-loxP system, Pain behavior assays, Lipidomics analysis
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