Informace o publikaci

Kolmer cells and their immunophenotyping in the rat choroid plexus after peripheral nerve injury

Název česky Kolmerovy buňky a jejich imunofenotypizace po poškození periferního nervu laboratorního potkana


Rok publikování 2015
Druh Konferenční abstrakty
Fakulta / Pracoviště MU

Lékařská fakulta

Popis Aim. The unilateral chronical constriction injury (CCI) used as a neuropathic pain model causes the elevation of proinflammatory cytokines levels not only in the structures directly related with damaged nerve but also in remote structures of central nervous system (CNS). The way how the neuroinflammatory molecules affect CNS is not completely clear. We purpose that one of the possible pathways for spread of neuroinflammation could be over the blood-cerebrospinal fluid barrier localized in choroid plexus (CP). CP is formed by highly vascularized stromal core with fenestrated capillaries covered by cuboidal cells on the ventricular side responsible for cerebrospinal fluid secretion. Epiplexal Kolmer cells (KC) are attached on the surface of the cuboidal cells. They are known as the scavenger cells processing the signals from blood to cerebrospinal fluid. Therefore, the aim of our study was to investigate changes of KC and CP after peripheral nerve injury. Methods. Twelve Wistar male rats were used in our experiments. Rats were anesthetized with a mixture of ketamine and xylazine administered intraperitoneally. CCI of the left sciatic nerve was performed by three ligatures that reduced the nerve diameter by approximately one-third. The animals were exposed to CCI for 3 (n=5) and 21 (n=5) days, two rats were naive. After time of survival, animals were sacrificed in CO2, perfused transcardially by Zamboni´s fixative; the brain was removed and fixed for three days. Immunohistochemical detection for resident (ED2) and activated (ED1) macrophages and dendritic cells (OX-42) was performed on coronal cryostat sections through the brain. Results. Immunostaining for ED1 showed activated macrophages in the stroma of CP and in epiplexal position. The number of ED1+ cells in CP increased with duration of nerve compression whereas the most ED1+ cells were found in epiplexal position after 21 days of nerve compression. Immunohistochemical detection for OX42+ showed the presentation of cells only in epiplexal position not in a stroma. Their number gradually increased respecting the time of CCI. KC positive for ED2 were found in CCI operated animals but not in naive rats. Conclusion. We demonstrated that population of KC is formed by cells with different immunophenotypes namely ED1, ED2 and OX42. We can conclude that the number of KC increased after peripheral nerve injury. KC are blood derived therefore the changes of their number could be caused by alteration of tight junctions that are found between the cuboidal cells. These changes could result in a spread of neuroinflammatory reaction from peripheral nervous system to the CNS structures.
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