Informace o publikaci
Study of changes in the rat choroid plexus after peripheral nerve injury using fluorescent conjugated dextran
| Název česky | Studium změn plexus choroideus laboratorního potkana po poškození periferní nervu pomocí fluorescenčně značeného dextranu |
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| Autoři | |
| Rok publikování | 2015 |
| Druh | Konferenční abstrakty |
| Fakulta / Pracoviště MU | |
| Citace | |
| Popis | Aim. Peripheral nerve injury can lead to cellular and molecular changes in the peripheral and central nervous system structures which are not directly related with damaged nerve. We suppose that these structures can be influenced by damage associated molecular patterns (DAMPs) produced by Wallerian degeneration and diffused via blood-cerebrospinal fluid barrier (B-CSF-B). This barrier is present in the choroid plexus (CP) of brain ventricles. CP consists of highly vascularized stromal core with fenestrated capillaries and cuboidal cells covering the ventricular side. Epiplexal Kolmer cells (KC) attached on the surface of the cuboidal cells are involved in neuroimmunological regulations. The aim of our study was to investigate the changes of CP after peripheral nerve injury. For this purpose we used intravenously injected fluorescent conjugated dextran FluoroEmerald (FE) with different time of circulation. Methods. Twenty Wistar rats (male, 250-300g) were anaesthetized with a mixture of ketamine and xylazine and unilateral chronic constriction injury (CCI) of the sciatic nerve was performed. CCI operated rats were left to survive for 3 days (3D) (n=8) and 21 days (21D) (n=8). Four naive rats were used as control. After time of CCI survival the FE was intravenously applied after anesthesia to the left external jugular vein. Time of FE circulation was 5 hours (n=4) and 18 hours (n=4) in each period of CCI survival. Then, the rats were deeply anaesthetized, perfused transcardially by Zamboni´s fixative and the brains were removed and fixed for three days. Coronal cryostat sections (20 µm) were cut through the lateral and third ventricles. Distribution of FE and simultaneous immunohistochemical detection of resident (ED2) and activated (ED1) macrophages, antigen presenting cells (APC; MHC-II), T-cells (OX-52) and dendritic cells (OX-42) were analyzed using fluorescence microscope. Results. FE particles were found inside the cuboidal cells, the immune stromal cells and the KC. Statistically significant increase of number of FE+ cells was found in CP after 3 and 21 days of CCI and FE circulation for 18, but not for 5hours. Most of FE+ cells were found in CP 21 days from CCI and circulation for 18 hours. FE particles were detected inside stromal cells of the CP which displayed immunophenotypes of activated macrophages (ED1+) and antigen presenting cells (MHC-II+). KC without FE particles were immunostained for ED1, MHC-II and OX42. Number of OX42+ cells in CP increased with duration of nerve compression. FE positive KC were simultaneously positive for ED2 and OX52, respectively. Conclusion. CP responds to the chronic peripheral nerve damage with presence of FE+ cells in the stroma. Therefore, we assume that CP is a possible way how proinflammatory molecules from peripheral nerve injury could spread into the central nervous system. These CP changes occur with prolonged peripheral nerve damage by contrast to dorsal root ganglia. We also demonstrated increased penetration of immune cells through B-CSF-B induced by peripheral nerve injury. These changes could be caused by alteration in tight junctions. |
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