Fig 1: HIVBa−L gp120 induces PGE2 expression in microglia via PTGS2 and PTGES. A–C MMG were pretreated with 10 nM SC560, 100 nM celecoxib, or vehicle for 1 h, then exposed to 2 ng mL⁻¹ gp120 or vehicle (n = 4). A After 24 h, PGE₂ levels were measured by competitive immunoassay. B TREM1 mRNA was quantified at 6 h by RT-qPCR. C TREM1 protein was quantified at 24 h by western blot. Left: representative blots with ACTB as loading control. Right: densitometric analysis (n = 4). D–F MMG were pretreated with 100 nM MF63 or vehicle for 1 h, then treated with gp120 or vehicle (n = 4). D PGE₂ was measured at 24 h. E TREM1 protein was quantified at 24 h by western blot. Left: representative blots with ACTB as loading control. Right: densitometric analysis (n = 4). G MMG were treated with gp120 or vehicle and harvested at multiple time points. PTGS2 and TREM1 mRNA were assessed by RT-qPCR, and PGE₂ by immunoassay (n = 4). H Conditioned media were collected at early and late time points following gp120 or vehicle exposure and analysed for extracellular WARS1 by ELISA, with non-zero time points plotted on a log10 time scale (n = 4). I MMG were treated with PGE₂ or vehicle. TREM1 mRNA was measured at 6 h (n = 4). J MMG were pretreated with 100 nM SC51322 (PTGER1/EP1 antagonist), 100 nM PF 04418948 (PTGER2/EP2 antagonist), 100 nM L-798,106 (PTGER3/EP3 antagonist), 100 nM E7046 (PTGER4/EP4 antagonist), or vehicle for 1 h before gp120 or vehicle exposure. TREM1 mRNA was quantified at 6 h by RT-qPCR (n = 4). Data are shown as mean ± SD; *p < 0.05