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Quinpramine Ameliorates Rat Experimental Autoimmune Neuritis and Redistributes MHC Class II Molecules
Activation of inflammatory cells is central to the pathogenesis of autoimmune demyelinating diseases of the peripheral nervous system. The novel chimeric compound quinpramine—generated from imipramine and quinacrine—redistributes cholesterol rich membrane domains to intracellular compartments. We st...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3116892/ https://www.ncbi.nlm.nih.gov/pubmed/21698177 http://dx.doi.org/10.1371/journal.pone.0021223 |
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author | Meyer zu Hörste, Gerd Mausberg, Anne K. Müller, Johanna I. Lehmann, Helmar C. Löber, Stefan Gmeiner, Peter Hartung, Hans-Peter Stüve, Olaf Korth, Carsten Kieseier, Bernd C. |
author_facet | Meyer zu Hörste, Gerd Mausberg, Anne K. Müller, Johanna I. Lehmann, Helmar C. Löber, Stefan Gmeiner, Peter Hartung, Hans-Peter Stüve, Olaf Korth, Carsten Kieseier, Bernd C. |
author_sort | Meyer zu Hörste, Gerd |
collection | PubMed |
description | Activation of inflammatory cells is central to the pathogenesis of autoimmune demyelinating diseases of the peripheral nervous system. The novel chimeric compound quinpramine—generated from imipramine and quinacrine—redistributes cholesterol rich membrane domains to intracellular compartments. We studied the immunological and clinical effects of quinpramine in myelin homogenate induced Lewis rat experimental autoimmune neuritis (EAN), a model system for acute human inflammatory neuropathies, such as the Guillain-Barré syndrome. EAN animals develop paresis of all limbs due to autoimmune inflammation of peripheral nerves. Quinpramine treatment ameliorated clinical disease severity of EAN and infiltration of macrophages into peripheral nerves. It reduced expression of MHC class II molecules on antigen presenting cells and antigen specific T cell proliferation both in vitro and in vivo. Quinpramine exerted its anti-proliferatory effect on antigen presenting cells, but not on responder T cells. Our data suggest that quinpramine represents a candidate pharmaceutical for inflammatory neuropathies. |
format | Online Article Text |
id | pubmed-3116892 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-31168922011-06-22 Quinpramine Ameliorates Rat Experimental Autoimmune Neuritis and Redistributes MHC Class II Molecules Meyer zu Hörste, Gerd Mausberg, Anne K. Müller, Johanna I. Lehmann, Helmar C. Löber, Stefan Gmeiner, Peter Hartung, Hans-Peter Stüve, Olaf Korth, Carsten Kieseier, Bernd C. PLoS One Research Article Activation of inflammatory cells is central to the pathogenesis of autoimmune demyelinating diseases of the peripheral nervous system. The novel chimeric compound quinpramine—generated from imipramine and quinacrine—redistributes cholesterol rich membrane domains to intracellular compartments. We studied the immunological and clinical effects of quinpramine in myelin homogenate induced Lewis rat experimental autoimmune neuritis (EAN), a model system for acute human inflammatory neuropathies, such as the Guillain-Barré syndrome. EAN animals develop paresis of all limbs due to autoimmune inflammation of peripheral nerves. Quinpramine treatment ameliorated clinical disease severity of EAN and infiltration of macrophages into peripheral nerves. It reduced expression of MHC class II molecules on antigen presenting cells and antigen specific T cell proliferation both in vitro and in vivo. Quinpramine exerted its anti-proliferatory effect on antigen presenting cells, but not on responder T cells. Our data suggest that quinpramine represents a candidate pharmaceutical for inflammatory neuropathies. Public Library of Science 2011-06-16 /pmc/articles/PMC3116892/ /pubmed/21698177 http://dx.doi.org/10.1371/journal.pone.0021223 Text en Meyer zu Hörste et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Meyer zu Hörste, Gerd Mausberg, Anne K. Müller, Johanna I. Lehmann, Helmar C. Löber, Stefan Gmeiner, Peter Hartung, Hans-Peter Stüve, Olaf Korth, Carsten Kieseier, Bernd C. Quinpramine Ameliorates Rat Experimental Autoimmune Neuritis and Redistributes MHC Class II Molecules |
title | Quinpramine Ameliorates Rat Experimental Autoimmune Neuritis and Redistributes MHC Class II Molecules |
title_full | Quinpramine Ameliorates Rat Experimental Autoimmune Neuritis and Redistributes MHC Class II Molecules |
title_fullStr | Quinpramine Ameliorates Rat Experimental Autoimmune Neuritis and Redistributes MHC Class II Molecules |
title_full_unstemmed | Quinpramine Ameliorates Rat Experimental Autoimmune Neuritis and Redistributes MHC Class II Molecules |
title_short | Quinpramine Ameliorates Rat Experimental Autoimmune Neuritis and Redistributes MHC Class II Molecules |
title_sort | quinpramine ameliorates rat experimental autoimmune neuritis and redistributes mhc class ii molecules |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3116892/ https://www.ncbi.nlm.nih.gov/pubmed/21698177 http://dx.doi.org/10.1371/journal.pone.0021223 |
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