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Figure 3 | Journal of Neuroinflammation

Figure 3

From: Improvement of spinal non-viral IL-10gene delivery by D-mannose as a transgene adjuvant to control chronic neuropathic pain

Figure 3

D-mannose generates short-term reversal of allodynia, an M2 polarized phenotype and improved pDNA-IL-10 transgene uptake in macrophage cell cultures. (A and B) after baseline (BL) assessment, all animals underwent chronic constriction injury (CCI) surgery resulting in allodynia by day 10. On day 10, animals were given a single i.t. injection of D-mannose (50, 5, or 0.5 μg; closed squares, closed circles, or closed diamonds respectively) or equivolume saline (n = 3 to 4 per group). Saline-treated animals (open diamonds) remained bilaterally allodynic. Treatment with D-mannose (50 μg, n = 3) resulted in bilateral partial reversal from allodynia that returned by day 20 following i.t. injection (ipsilateral, F(3,70) = 15.87; P < 0.0005; contralateral F(3,70) = 20.40; P < 0.0001). Black arrows indicate i.t. injection. (C-F) cultured Raw 264.7 mouse macrophage cells were pretreated with D-mannose (100 mM) followed by a two-hour incubation with a combination of D-mannose (100 mM) and lipopolysaccharide (LPS) (10 ng). (C) compared to control treatment (No Tx = no treatment; Mann = D-mannose), LPS-stimulated cells given D-mannose treatment resulted in significantly increased mouse IL-10 protein levels, (D) almost complete ablation of IL-1β levels, (E) significantly reduced TNF-α protein levels, and (F) reduced NO production. (G) cultured Raw 264.7 mouse macrophage cells treated with IL-4 did not improve pDNA-IL-10 transgene expression, however, (H) D-mannose generated a robust dose-dependent increase in pDNA-IL-10 transgene expression. *P < 0.05; **P < 0.01; ***P < 0.0001.

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