open access

Vol 56, No 3 (2018)
Original paper
Submitted: 2018-06-05
Accepted: 2018-07-30
Published online: 2018-08-30
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Immunohistochemical analysis of spinal cord components in mouse model of experimental autoimmune encephalomyelitis

Grazyna Pyka-Fosciak1, Mariusz Stasiolek2, Jan A. Litwin1
DOI: 10.5603/FHC.a2018.0018
·
Pubmed: 30187907
·
Folia Histochem Cytobiol 2018;56(3):151-158.
Affiliations
  1. Department of Histology, Jagiellonian University Medical College, Krakow, Poland
  2. Department of Neurology, Medical University of Lodz, Lodz, Poland

open access

Vol 56, No 3 (2018)
ORIGINAL PAPERS
Submitted: 2018-06-05
Accepted: 2018-07-30
Published online: 2018-08-30

Abstract

Introduction. Experimental autoimmune encephalomyelitis (EAE) is a widely used animal model for studying immunopathology of multiple sclerosis (MS) because it repeats the hallmarks of the human disease, such as focal inflammation and demyelination of the central nervous system, subsequently leading to axonal and neuronal loss. The interrelationships, timing and sequence of different pathological processes that lead to histologically observed lesions in SM are still incompletely understood.
Material and methods. EAE was induced in female C57Bl/6 mice by active immunization with MOG35-55 antigen. Development of the neurological symptoms in the animals was monitored and on that basis spinal cords were collected in three successive phases of the disease (onset, peak, chronic). Total leukocytes, T cells, macrophages/microglia, oligodendrocytes, damaged axons and surviving neuronal cell bodies were visualized using appropriate immunohistochemical markers and their density was quantitatively assessed using image analysis software.
Results. The density of all studied cells except neurons was significantly higher in EAE mice than in the control mice. The density of total leukocytes, T cells, and damaged axons increased from the onset to the peak phase and decreased in the chronic phase to reach values lower than those in the peak phase. The density of macrophages/microglia increased in the peak phase and remained at the elevated level in the chronic phase. Oligodendrocytes showed the highest density in the onset phase and gradually decreased afterwards. The density of neuronal cell bodies decreased only in the chronic phase of the disease.
Conclusions. In mouse model of EAE, inflammatory cells predominate in the early phases of the disease. This study shows for the first time that inflammation precedes oligodendrocyte death and neuronal loss and that macrophages/ microglia are the only cells persisting in large numbers in the chronic phase of the disease, probably because of the switch from proinflammatory to anti-inflammatory phenotype.

Abstract

Introduction. Experimental autoimmune encephalomyelitis (EAE) is a widely used animal model for studying immunopathology of multiple sclerosis (MS) because it repeats the hallmarks of the human disease, such as focal inflammation and demyelination of the central nervous system, subsequently leading to axonal and neuronal loss. The interrelationships, timing and sequence of different pathological processes that lead to histologically observed lesions in SM are still incompletely understood.
Material and methods. EAE was induced in female C57Bl/6 mice by active immunization with MOG35-55 antigen. Development of the neurological symptoms in the animals was monitored and on that basis spinal cords were collected in three successive phases of the disease (onset, peak, chronic). Total leukocytes, T cells, macrophages/microglia, oligodendrocytes, damaged axons and surviving neuronal cell bodies were visualized using appropriate immunohistochemical markers and their density was quantitatively assessed using image analysis software.
Results. The density of all studied cells except neurons was significantly higher in EAE mice than in the control mice. The density of total leukocytes, T cells, and damaged axons increased from the onset to the peak phase and decreased in the chronic phase to reach values lower than those in the peak phase. The density of macrophages/microglia increased in the peak phase and remained at the elevated level in the chronic phase. Oligodendrocytes showed the highest density in the onset phase and gradually decreased afterwards. The density of neuronal cell bodies decreased only in the chronic phase of the disease.
Conclusions. In mouse model of EAE, inflammatory cells predominate in the early phases of the disease. This study shows for the first time that inflammation precedes oligodendrocyte death and neuronal loss and that macrophages/ microglia are the only cells persisting in large numbers in the chronic phase of the disease, probably because of the switch from proinflammatory to anti-inflammatory phenotype.

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Keywords

EAE; spinal cord; leukocytes; T cells; macrophages; microglia; oligodendrocytes; neuronal damage; immunohistochemistry

About this article
Title

Immunohistochemical analysis of spinal cord components in mouse model of experimental autoimmune encephalomyelitis

Journal

Folia Histochemica et Cytobiologica

Issue

Vol 56, No 3 (2018)

Article type

Original paper

Pages

151-158

Published online

2018-08-30

DOI

10.5603/FHC.a2018.0018

Pubmed

30187907

Bibliographic record

Folia Histochem Cytobiol 2018;56(3):151-158.

Keywords

EAE
spinal cord
leukocytes
T cells
macrophages
microglia
oligodendrocytes
neuronal damage
immunohistochemistry

Authors

Grazyna Pyka-Fosciak
Mariusz Stasiolek
Jan A. Litwin

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