Astrocytic hypertrophy: An important pathological feature of chronic experimental autoimmune encephalitis in aged rats

Experimental autoimmune encephalomyelitis (EAE) was induced in young (2–3 month old), middle-aged (12–13 month old) and geriatric (24–26 month old) Lewis (JC) rats by active immunisation with myelin basic protein (MBP) in complete Freund's adjuvant (CFA). It was found that aged Lewis (JC) rats...

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Veröffentlicht in:Journal of neuroimmunology 1993-11, Vol.48 (2), p.121-134
Hauptverfasser: Ludowyk, Patricia A., Hughes, Wendy, Hugh, Andrew, Willenberg, David O., Rockett, Kirk A., Parish, Christopher R.
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container_issue 2
container_start_page 121
container_title Journal of neuroimmunology
container_volume 48
creator Ludowyk, Patricia A.
Hughes, Wendy
Hugh, Andrew
Willenberg, David O.
Rockett, Kirk A.
Parish, Christopher R.
description Experimental autoimmune encephalomyelitis (EAE) was induced in young (2–3 month old), middle-aged (12–13 month old) and geriatric (24–26 month old) Lewis (JC) rats by active immunisation with myelin basic protein (MBP) in complete Freund's adjuvant (CFA). It was found that aged Lewis (JC) rats developed a more chronic form of EAE than younger rats of the same strain, a phenomenon observed in both male and female rats despite males developing more severe disease than females at all ages. Middle-aged recipients also developed more severe disease than young recipients when EAE was induced by the adoptive transfer of lymphocytes from actively immunised young donors, suggesting that disease chronicity in middle-aged animals is a property of the central nervous system (CNS) milieu. Histological studies demonstrated that disease chronicity did not correlate with the number of inflammatory lesions in the CNS, young animals containing substantial numbers of CNS lesions following recovery and lesions being largely absent from middle-aged animals which still exhibited signs of disease. No significant differences were found in the degree of fibrin deposition or demyelination between young and middle-aged or symptomatic and asymptomatic animals. However, astrocytic hypertrophy was found to correlate with manifestation of disease in both young and middle-aged animals and in particular with disease chronicity in middle-aged animals. In parallel studies, no significant differences were found in the levels of the inflammatory mediators tumor necrosis factor (TNF)-α, prostaglandin E (PGE) 2, reactive nitrogen intermediates (RNI) and corticosterone in young and middle-aged animals. However, markedly elevated corticosterone levels were found in both young and middle-aged animals with the development of clinical signs which returned to baseline levels with the resolution of clinical signs. Elevated levels of RNI were evident in animals immediately prior to and during the early stages of symptomatic EAE. Although these results suggest that nitric oxide may play a role in the pathogenesis of disease, whereas corticosterone may play a role in the immunoregulation of the disease, these factors cannot explain differences in disease chronicity evident in middle-aged animals. Based on the results presented in this paper, it is proposed that the neurological deficit of chronic EAE in middle-aged animals may be caused by astrocytic hypertrophy with the resolution of this CNS response b
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However, astrocytic hypertrophy was found to correlate with manifestation of disease in both young and middle-aged animals and in particular with disease chronicity in middle-aged animals. In parallel studies, no significant differences were found in the levels of the inflammatory mediators tumor necrosis factor (TNF)-α, prostaglandin E (PGE) 2, reactive nitrogen intermediates (RNI) and corticosterone in young and middle-aged animals. However, markedly elevated corticosterone levels were found in both young and middle-aged animals with the development of clinical signs which returned to baseline levels with the resolution of clinical signs. Elevated levels of RNI were evident in animals immediately prior to and during the early stages of symptomatic EAE. 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Animal models</subject><subject>Experimental autoimmune encephalomyelitis</subject><subject>Female</subject><subject>Hypertrophy</subject><subject>Immunopathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myelin Basic Protein - immunology</subject><subject>Rats</subject><subject>Rats, Inbred Lew</subject><subject>Spinal Cord - pathology</subject><issn>0165-5728</issn><issn>1872-8421</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUuLFDEUhYMoY9v6DxSyENFFaR6VqsSF0Ay-YMCNbmYT0qmbqUhVUiapwf73pu2ml7oIl3C-c0nOQeg5JW8pod27ekQjeiZfK_5GESrb5vYB2lDZs0a2jD5EmwvyGD3J-SchVPBWXaGrvlO8F3SD7ne5pGgPxVs8HhZI9baMh_d4F7Cfl5iKCQUvpoxxinfemgk7MGVNgKPDdkwxVCf8rk4_QyhVN2uJfp7XABiChWU0ky8-Yx-wuYMBJ1PyU_TImSnDs_Pcoh-fPn6__tLcfPv89Xp309i2k6Vxzsk9pdANXA4WRJ1CEWcpUyA7QpRwynGoEwQFaV0nBzYw3lunKNszvkWvTnuXFH-tkIuefbYwTSZAXLPuO9JKJuh_QdopJrqa2ha1J9CmmHMCp5f6c5MOmhJ97EUfQ9fH0LXi-m8v-rbaXpz3r_sZhovpXETVX551k2vILplgfb5gXJGetbJiH04Y1NDuPSSdrT-mPPgEtugh-n-_4w-466xz</recordid><startdate>19931101</startdate><enddate>19931101</enddate><creator>Ludowyk, Patricia A.</creator><creator>Hughes, Wendy</creator><creator>Hugh, Andrew</creator><creator>Willenberg, David O.</creator><creator>Rockett, Kirk A.</creator><creator>Parish, Christopher R.</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>19931101</creationdate><title>Astrocytic hypertrophy: An important pathological feature of chronic experimental autoimmune encephalitis in aged rats</title><author>Ludowyk, Patricia A. ; Hughes, Wendy ; Hugh, Andrew ; Willenberg, David O. ; Rockett, Kirk A. ; Parish, Christopher R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c468t-fff8b11e6d38dce56d3590fc129e860095f9f3e095e51e8cf68d2d237cf912b23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Age</topic><topic>Age Factors</topic><topic>Animals</topic><topic>Astrocytes - pathology</topic><topic>Astrocytic hypertrophy</topic><topic>Biological and medical sciences</topic><topic>Encephalomyelitis, Autoimmune, Experimental - pathology</topic><topic>Experimental and animal immunopathology. 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It was found that aged Lewis (JC) rats developed a more chronic form of EAE than younger rats of the same strain, a phenomenon observed in both male and female rats despite males developing more severe disease than females at all ages. Middle-aged recipients also developed more severe disease than young recipients when EAE was induced by the adoptive transfer of lymphocytes from actively immunised young donors, suggesting that disease chronicity in middle-aged animals is a property of the central nervous system (CNS) milieu. Histological studies demonstrated that disease chronicity did not correlate with the number of inflammatory lesions in the CNS, young animals containing substantial numbers of CNS lesions following recovery and lesions being largely absent from middle-aged animals which still exhibited signs of disease. No significant differences were found in the degree of fibrin deposition or demyelination between young and middle-aged or symptomatic and asymptomatic animals. 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Although these results suggest that nitric oxide may play a role in the pathogenesis of disease, whereas corticosterone may play a role in the immunoregulation of the disease, these factors cannot explain differences in disease chronicity evident in middle-aged animals. Based on the results presented in this paper, it is proposed that the neurological deficit of chronic EAE in middle-aged animals may be caused by astrocytic hypertrophy with the resolution of this CNS response being a major factor contributing to recovery from the disease in animals of all ages.</abstract><cop>London</cop><cop>Amsterdam</cop><cop>New York, NY</cop><pub>Elsevier B.V</pub><pmid>7693751</pmid><doi>10.1016/0165-5728(93)90184-Z</doi><tpages>14</tpages></addata></record>
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subjects Age
Age Factors
Animals
Astrocytes - pathology
Astrocytic hypertrophy
Biological and medical sciences
Encephalomyelitis, Autoimmune, Experimental - pathology
Experimental and animal immunopathology. Animal models
Experimental autoimmune encephalomyelitis
Female
Hypertrophy
Immunopathology
Male
Medical sciences
Myelin Basic Protein - immunology
Rats
Rats, Inbred Lew
Spinal Cord - pathology
title Astrocytic hypertrophy: An important pathological feature of chronic experimental autoimmune encephalitis in aged rats
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