Figure 5.
Figure 5. PGE 2 rescues the migratory pattern of CsA-treated DCs. (A) CsA inhibits LPS-induced COX-2 expression. Murine bone marrow–derived DCs were treated as indicated and COX-2 expression assayed by RT-PCR and Western blot assays. CsA/LPS: Day 5 DCs were treated with CsA (1 μg/mL) for 12 hours, and then LPS (100 ng/mL) was added for the final 12 hours. (B) CsA inhibits PGE2 production of LPS-stimulated murine DCs. (C) Western blot assay of CKR expression by murine BMDCs following supplementation with PGE2 (1 μg/mL). (D) FACS analysis of CKR expression on PGE2-supplemented human MoDCs. Results presented as mean fluorescence intensity (MFI) ± SE. (E-F) PGE2 restores responsiveness of CsA-treated murine BMDCs (E) and human MoDCs (F) to MIP-1α or MIP-3β. In panels C-F, day 5 DCs were treated by CsA (1 μg/mL) for 48 hours and stimulated by LPS (100 ng/mL) in the last 24 hours. Results in panels B and D are expressed as means ± SEM; results in panels E-F are expressed as means ± SD.

PGE2rescues the migratory pattern of CsA-treated DCs. (A) CsA inhibits LPS-induced COX-2 expression. Murine bone marrow–derived DCs were treated as indicated and COX-2 expression assayed by RT-PCR and Western blot assays. CsA/LPS: Day 5 DCs were treated with CsA (1 μg/mL) for 12 hours, and then LPS (100 ng/mL) was added for the final 12 hours. (B) CsA inhibits PGE2 production of LPS-stimulated murine DCs. (C) Western blot assay of CKR expression by murine BMDCs following supplementation with PGE2 (1 μg/mL). (D) FACS analysis of CKR expression on PGE2-supplemented human MoDCs. Results presented as mean fluorescence intensity (MFI) ± SE. (E-F) PGE2 restores responsiveness of CsA-treated murine BMDCs (E) and human MoDCs (F) to MIP-1α or MIP-3β. In panels C-F, day 5 DCs were treated by CsA (1 μg/mL) for 48 hours and stimulated by LPS (100 ng/mL) in the last 24 hours. Results in panels B and D are expressed as means ± SEM; results in panels E-F are expressed as means ± SD.

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