Prostaglandin E2 Affects Differently the Release of Inflammatory Mediators from Resident Macrophages by LPS and Muramyl Tripeptides
LPS and MTP-PE (liposome-encapsulated N-acetylmuramyl-L-alanyl-D-isoglutaminyl-L-alanine-2-:[1',2'-dipalmitoyl-sni-glycero-3-(hydroxy-phosphoryl-oxyl)] etylamide) induce in liver macrophages a synthesis and release of TNF-α, nitric oxide and prostanoids. Both agents induce an expression of...
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| Format: | Article |
| Language: | English |
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Wiley
1999-01-01
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| Series: | Mediators of Inflammation |
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| Online Access: | http://dx.doi.org/10.1080/09629359990306 |
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| _version_ | 1850178450748342272 |
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| author | Peter Dieter Ute Hempel Sabine Kamionka Angelika Kolada Birgit Malessa Edith Fitzke Thuy-Anh Tran-Thi |
| author_facet | Peter Dieter Ute Hempel Sabine Kamionka Angelika Kolada Birgit Malessa Edith Fitzke Thuy-Anh Tran-Thi |
| author_sort | Peter Dieter |
| collection | DOAJ |
| description | LPS and MTP-PE (liposome-encapsulated N-acetylmuramyl-L-alanyl-D-isoglutaminyl-L-alanine-2-:[1',2'-dipalmitoyl-sni-glycero-3-(hydroxy-phosphoryl-oxyl)] etylamide) induce in liver macrophages a synthesis and release of TNF-α, nitric oxide and prostanoids. Both agents induce an expression of mRNA's encoding TNF-α, inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2, and of corresponding proteins. LPS and MTP-PE induce a rapid activation of the extracellular regulated kinase (ERK) isoenzymes-1 and -2. Inhibition of map kinase isoenzymes leads to a decreased release of TNF-α, nitric oxide and prostaglandin (PG) E2 after both agents. The transcription factors NF-κB and AP-1 are strongly activated by LPS within 30 minutes. MTP-PE induces a weak activation of both transcription factors only after 5 hours. Inhibition of NF-κB inhibits the LPS- but not the MTP-PE-induced release of TNF-α, nitric oxide and PGE2. PGE2 release after LPS is higher than after MTP-PE. Exogenously added PGE2 inhibits the activation of map kinase and TNF-α release by LPS, but not by MTP-PE. Release of nitric oxide after LPS and MTP-PE is enhanced after prior addition of PGE2. PGD2 is without any effect. MTP-PE, but not LPS, induces a cytotoxicity of Kupffer cells against P815 tumor target cells. The MTP-PE-induced cytotoxicity is reduced by TNF-α neutralizing antibodies, indicating the involvement of TNF-α. Thus our results suggest that the different potencies of LPS and MTP-PE as immunomodulators probably result from different actions on Kupffer cells, resulting in differences in the amounts and kinetics of released TNF-α and PGE2, and that PGE2 plays an important regulatory role in the action of LPS, but not in the actions of MTP-PE. |
| format | Article |
| id | doaj-art-bc5a5b0c699344f88f8aa50f2b5d8e14 |
| institution | OA Journals |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 1999-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-bc5a5b0c699344f88f8aa50f2b5d8e142025-08-20T02:18:43ZengWileyMediators of Inflammation0962-93511466-18611999-01-018629530310.1080/09629359990306Prostaglandin E2 Affects Differently the Release of Inflammatory Mediators from Resident Macrophages by LPS and Muramyl TripeptidesPeter Dieter0Ute Hempel1Sabine Kamionka2Angelika Kolada3Birgit Malessa4Edith Fitzke5Thuy-Anh Tran-Thi6Institute of Physiological Chemistry, Medical Faculty, Dresden University of Technology, Karl-Marx-Strasse 3, Dresden D-01109, GermanyInstitute of Physiological Chemistry, Medical Faculty, Dresden University of Technology, Karl-Marx-Strasse 3, Dresden D-01109, GermanyInstitute of Physiological Chemistry, Medical Faculty, Dresden University of Technology, Karl-Marx-Strasse 3, Dresden D-01109, GermanyInstitute of Physiological Chemistry, Medical Faculty, Dresden University of Technology, Karl-Marx-Strasse 3, Dresden D-01109, GermanyInstitute of Physiological Chemistry, Medical Faculty, Dresden University of Technology, Karl-Marx-Strasse 3, Dresden D-01109, GermanyInstitute of Biochemistry and Molecular Biology, Albert-Ludwigs-University, Freiburg, GermanyInstitute of Biochemistry and Molecular Biology, Albert-Ludwigs-University, Freiburg, GermanyLPS and MTP-PE (liposome-encapsulated N-acetylmuramyl-L-alanyl-D-isoglutaminyl-L-alanine-2-:[1',2'-dipalmitoyl-sni-glycero-3-(hydroxy-phosphoryl-oxyl)] etylamide) induce in liver macrophages a synthesis and release of TNF-α, nitric oxide and prostanoids. Both agents induce an expression of mRNA's encoding TNF-α, inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2, and of corresponding proteins. LPS and MTP-PE induce a rapid activation of the extracellular regulated kinase (ERK) isoenzymes-1 and -2. Inhibition of map kinase isoenzymes leads to a decreased release of TNF-α, nitric oxide and prostaglandin (PG) E2 after both agents. The transcription factors NF-κB and AP-1 are strongly activated by LPS within 30 minutes. MTP-PE induces a weak activation of both transcription factors only after 5 hours. Inhibition of NF-κB inhibits the LPS- but not the MTP-PE-induced release of TNF-α, nitric oxide and PGE2. PGE2 release after LPS is higher than after MTP-PE. Exogenously added PGE2 inhibits the activation of map kinase and TNF-α release by LPS, but not by MTP-PE. Release of nitric oxide after LPS and MTP-PE is enhanced after prior addition of PGE2. PGD2 is without any effect. MTP-PE, but not LPS, induces a cytotoxicity of Kupffer cells against P815 tumor target cells. The MTP-PE-induced cytotoxicity is reduced by TNF-α neutralizing antibodies, indicating the involvement of TNF-α. Thus our results suggest that the different potencies of LPS and MTP-PE as immunomodulators probably result from different actions on Kupffer cells, resulting in differences in the amounts and kinetics of released TNF-α and PGE2, and that PGE2 plays an important regulatory role in the action of LPS, but not in the actions of MTP-PE.http://dx.doi.org/10.1080/09629359990306LPSMacrophagesMuramyl tripeptidesCytokines Eicosanoids. |
| spellingShingle | Peter Dieter Ute Hempel Sabine Kamionka Angelika Kolada Birgit Malessa Edith Fitzke Thuy-Anh Tran-Thi Prostaglandin E2 Affects Differently the Release of Inflammatory Mediators from Resident Macrophages by LPS and Muramyl Tripeptides Mediators of Inflammation LPS Macrophages Muramyl tripeptides Cytokines Eicosanoids. |
| title | Prostaglandin E2 Affects Differently the Release of Inflammatory Mediators from Resident Macrophages by LPS and Muramyl Tripeptides |
| title_full | Prostaglandin E2 Affects Differently the Release of Inflammatory Mediators from Resident Macrophages by LPS and Muramyl Tripeptides |
| title_fullStr | Prostaglandin E2 Affects Differently the Release of Inflammatory Mediators from Resident Macrophages by LPS and Muramyl Tripeptides |
| title_full_unstemmed | Prostaglandin E2 Affects Differently the Release of Inflammatory Mediators from Resident Macrophages by LPS and Muramyl Tripeptides |
| title_short | Prostaglandin E2 Affects Differently the Release of Inflammatory Mediators from Resident Macrophages by LPS and Muramyl Tripeptides |
| title_sort | prostaglandin e2 affects differently the release of inflammatory mediators from resident macrophages by lps and muramyl tripeptides |
| topic | LPS Macrophages Muramyl tripeptides Cytokines Eicosanoids. |
| url | http://dx.doi.org/10.1080/09629359990306 |
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