PMID- 9669698
OWN - NLM
STAT- MEDLINE
DCOM- 19980909
LR  - 20240426
IS  - 1015-6305 (Print)
IS  - 1750-3639 (Electronic)
IS  - 1015-6305 (Linking)
VI  - 8
IP  - 3
DP  - 1998 Jul
TI  - Microvascular and cellular responses in the optic nerve of rats with acute 
      experimental allergic encephalomyelitis (EAE).
PG  - 475-86
AB  - The optic nerve of rats with EAE was examined at various times to determine the 
      integrity of the blood-brain barrier (BBB) and to assess monocyte-macrophage, T 
      cell, and microglial responses. In naive control animals, leakage of horseradish 
      peroxidase (HRP) and the presence of cells expressing major histocompatibility 
      complex (MHC) class II antigen were evident in the meninges of the retrobulbar 
      optic nerve. In rats with EAE, microglia in the region of the lamina cribrosa and 
      in the regions adjacent to the meninges became activated from day 7 to 8 
      postinduction (pi). HRP leakage was also evident in the region of the lamina 
      cribrosa from day 7 to 8 pi. On day 8 pi, infiltration of inflammatory cells and 
      Monastral blue leakage were apparent in the myelinated region of the optic nerve. 
      The intensity of these cellular and vascular changes peaked at day 12 pi, when 
      signs of clinical disease became manifest. Monocytes-macrophages expressing MHC 
      class II and the ED1 antigen, together with lymphocytes expressing the alphabetaT 
      cell receptor, constituted the major proportion of cells associated with 
      inflammatory lesions. Thus: (i) the inherent weakness of the BBB as well as the 
      presence of both antigen (myelin) and MHC class II+ cells in the retrobulbar 
      optic nerve are likely susceptibility factors for the frequent involvement of 
      this region in EAE and multiple sclerosis; and (ii) activation of microglia 
      occurs early in the pathogenesis of experimental optic neuritis.
FAU - Hu, P
AU  - Hu P
AD  - Department of Anatomy and Histology, Institute for Biomedical Research, 
      University of Sydney, NSW, Australia.
FAU - Pollard, J
AU  - Pollard J
FAU - Hunt, N
AU  - Hunt N
FAU - Taylor, J
AU  - Taylor J
FAU - Chan-Ling, T
AU  - Chan-Ling T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Switzerland
TA  - Brain Pathol
JT  - Brain pathology (Zurich, Switzerland)
JID - 9216781
RN  - 0 (Coloring Agents)
RN  - 0 (Histocompatibility Antigens Class II)
RN  - 0 (Indoles)
RN  - 0 (Myelin Basic Protein)
RN  - 0 (Organometallic Compounds)
RN  - 0 (Receptors, Antigen, T-Cell, alpha-beta)
RN  - 3VEX9T7UT5 (copper phthalocyanine)
RN  - EC 1.11.1.- (Horseradish Peroxidase)
SB  - IM
MH  - Animals
MH  - Blood-Brain Barrier/drug effects/*physiology
MH  - CD4-Positive T-Lymphocytes/immunology
MH  - CD8-Positive T-Lymphocytes/immunology
MH  - Coloring Agents
MH  - Encephalomyelitis, Autoimmune, Experimental/chemically 
      induced/immunology/*pathology
MH  - Histocompatibility Antigens Class II/metabolism
MH  - Horseradish Peroxidase
MH  - Immunohistochemistry
MH  - Indoles
MH  - Lymphocyte Subsets/immunology
MH  - Macrophages/immunology
MH  - Male
MH  - Microcirculation/pathology
MH  - Microglia/metabolism
MH  - Monocytes/immunology
MH  - Myelin Basic Protein/pharmacology
MH  - Myelin Sheath/pathology
MH  - Optic Nerve/*blood supply/immunology/metabolism/*pathology
MH  - Organometallic Compounds
MH  - Rats
MH  - Rats, Inbred Lew
MH  - Receptors, Antigen, T-Cell, alpha-beta/immunology
MH  - Time Factors
PMC - PMC8098482
EDAT- 1998/07/21 00:00
MHDA- 1998/07/21 00:01
PMCR- 2006/04/05
CRDT- 1998/07/21 00:00
PHST- 1998/07/21 00:00 [pubmed]
PHST- 1998/07/21 00:01 [medline]
PHST- 1998/07/21 00:00 [entrez]
PHST- 2006/04/05 00:00 [pmc-release]
AID - BPA475 [pii]
AID - 10.1111/j.1750-3639.1998.tb00169.x [doi]
PST - ppublish
SO  - Brain Pathol. 1998 Jul;8(3):475-86. doi: 10.1111/j.1750-3639.1998.tb00169.x.