Cell death of ED1+ cells in the central nervous system of Dark Agouti rats at the peak of experimental autoimmune encephalitis
2015
Autori:
Nikolovski, NedaLavrnja, Irena
Wendrich, Katrin
Momčilović, Miljana
Paquet-Durand, François
Trifunović, Dragana
Miljković, Đorđe
Ostala autorstva
Lukić, MiodragJonjic, Stipan
Nikolich-Zugich, Janko
Tip dokumenta:
Konferencijski prilog (Objavljena verzija)
,
© 2015 by the Immunological Society of Serbia
Metapodaci
Prikaz svih podataka o dokumentuApstrakt:
Infiltration of macrophages into the central nervous system (CNS), as well
as activation of microglia is a hallmark of multiple sclerosis and its animal
model - experimental autoimmune encephalomyelitis (EAE). Cell death in
EAE has been demonstrated as an essential mechanism in the local
regulation of the inflammatory reaction, but also as one of the major factors
contributing to the destruction of the CNS tissue. Here, cell death of ED1+
cells (macrophages/microglia) in the spinal cord of EAE rats was
investigated. Cell death in general was assessed using the TUNEL assay,
while cleaved caspase-3 immunostaining was employed as the marker of
“classical” apoptosis. Dark Agouti (DA) rats were immunized with spinal
cord homogenate emulsified in complete Freund's adjuvant. Infiltrates of
immune cells were detected both in white matter (WM) and grey matter
(GM) of spinal cords in DA rats at the peak of EAE. ED1+, TUNEL+ and
caspase-3+ cells were detected within, but also outside the infiltrates. While
there were no differences in the proportion of TUNEL+ ED1+ cells between
infiltrates and non-infiltrated areas in WM, there were more ED1+TUNEL+
cells in GM in infiltrates than in non–infiltrated areas. A similar distribution
was observed for ED1+caspase-3+ cells. The observed discrepancy in
distribution of dead ED1+ cells in infiltrates and non-infiltrated areas in GM
and WM of spinal cord indicated that differential spatial regulation of
macrophage/microglia cell death occurred in DA rats. These findings
contribute to the understanding of pathogenesis of EAE in DA rats. It also
opens new perspectives for a research aiming at more efficient treatment of
multiple sclerosis.
Finansiranje / projekti:
- Ćelijska i molekulska osnova neuroinflamacije: potencijala ciljna mesta za translacionu medicinu i terapiju (RS-MESTD-Integrated and Interdisciplinary Research (IIR or III)-41014)
- Ćelijski i molekulski mehanizmi oporavka pacova od eksperimentalnog autoimunskog encefalomijelitisa (RS-MESTD-Basic Research (BR or ON)-173035)
- Molekularni mehanizmi fiziološke i farmakološke kontrole inflamacije i kancera (RS-MESTD-Basic Research (BR or ON)-173013)
U:
- Lukić M, Jonjic S, Nikolich-Zugich J, editors. 3rd Belgrade EFIS symposium on Immunoregulation: Immunity, Infection, Autoimmunity and Aging; 2015 May 24-27; Arandjelovac, Serbia. Belgrade: Immunological Society of Serbia; 2015. p. 67.