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| DC Field | Value | Language |
|---|---|---|
| dc.contributor.author | Zou, L. P. | en |
| dc.contributor.author | Pelidou, S. H. | en |
| dc.contributor.author | Abbas, N. | en |
| dc.contributor.author | Deretzi, G. | en |
| dc.contributor.author | Mix, E. | en |
| dc.contributor.author | Schaltzbeerg, M. | en |
| dc.contributor.author | Winblad, B. | en |
| dc.contributor.author | Zhu, J. | en |
| dc.date.accessioned | 2015-11-24T19:23:28Z | - |
| dc.date.available | 2015-11-24T19:23:28Z | - |
| dc.identifier.issn | 0165-5728 | - |
| dc.identifier.uri | https://olympias.lib.uoi.gr/jspui/handle/123456789/22311 | - |
| dc.rights | Default Licence | - |
| dc.subject | Animals | en |
| dc.subject | Antibodies | en |
| dc.subject | Chemokine CCL2/*biosynthesis/immunology | en |
| dc.subject | Chemokine CCL3 | en |
| dc.subject | Chemokine CCL4 | en |
| dc.subject | Chemokine CXCL2 | en |
| dc.subject | Disease Progression | en |
| dc.subject | Freund's Adjuvant | en |
| dc.subject | Immunization | en |
| dc.subject | Macrophage Inflammatory Proteins/*biosynthesis/immunology | en |
| dc.subject | Macrophages/chemistry/immunology | en |
| dc.subject | Male | en |
| dc.subject | Monokines/*biosynthesis/immunology | en |
| dc.subject | Neuritis, Autoimmune, Experimental/*immunology/pathology | en |
| dc.subject | Neutralization Tests | en |
| dc.subject | Polyradiculoneuropathy/immunology | en |
| dc.subject | Rats | en |
| dc.subject | Rats, Inbred Lew | en |
| dc.subject | Sciatic Nerve/immunology/metabolism/pathology | en |
| dc.subject | T-Lymphocytes/immunology | en |
| dc.title | Dynamics of production of MIP-1alpha, MCP-1 and MIP-2 and potential role of neutralization of these chemokines in the regulation of immune responses during experimental autoimmune neuritis in Lewis rats | en |
| heal.type | journalArticle | - |
| heal.type.en | Journal article | en |
| heal.type.el | Άρθρο Περιοδικού | el |
| heal.identifier.secondary | http://www.ncbi.nlm.nih.gov/pubmed/10430050 | - |
| heal.language | en | - |
| heal.access | campus | - |
| heal.recordProvider | Πανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικής | el |
| heal.publicationDate | 1999 | - |
| heal.abstract | Experimental autoimmune neuritis (EAN) is an inflammatory autoimmune demyelinating disease of the peripheral nervous system (PNS) and represents an animal model of Guillain-Barre syndrome (GBS), which is a major inflammatory demyelinating disease of the PNS in humans. In the present study, the dynamics of the expression of the chemokines macrophage inflammatory protein-1alpha (MIP-1alpha), MIP-2 and monocyte chemotactic protein-1 (MCP-1) were determined in the sciatic nerves of EAN rats. Additionally, the effect of neutralizing antibodies against MIP-1alpha, MIP-2 and MCP-1 on the clinical course of EAN and the chemokine expression was investigated. The maximum of MIP-1alpha positive cells in the sciatic nerves was seen on day 14 post immunization (p.i.) correlating with the development of severe clinical signs. Administration of an anti-MIP-1alpha antibody suppressed the clinical signs of EAN and inhibited inflammation and demyelination in the sciatic nerve. Peak numbers of MCP-1 positive cells in the sciatic nerves were detected on day 7 p.i. Administration of an anti-MCP-1 antibody caused a delay of onset of EAN. However, 4 of the 6 EAN rats receiving the anti-MCP-antibody showed the same degree of inflammatory cell infiltration and demyelination in the sciatic nerves as sham-treated EAN rats, whereas only 2 EAN rats had less inflammation and demyelination. The numbers of MIP-2 positive cells reached a maximum on day 21 p.i. Anti-MIP-2 antibody failed to suppress the clinical signs of EAN and the inflammation and demyelination in the sciatic nerves. Only administration of the anti-MIP-1alpha antibody resulted in a significant reduction in the number of chemokine (MIP-1alpha)-positive cells and ED1-positive macrophages in the sciatic nerves. The present results demonstrate that MIP-1alpha and MCP-1 may play a role in the immunopathogenesis of EAN, and that MIP-1alpha induced trafficking of inflammatory cells can be inhibited by immunoneutralization. Further elucidation of the regulation and coordination of MIP-1alpha and MCP-1 production may lead to new therapeutic approaches to GBS in humans. | en |
| heal.journalName | J Neuroimmunol | en |
| heal.journalType | peer-reviewed | - |
| heal.fullTextAvailability | TRUE | - |
| Appears in Collections: | Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ | |
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