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Roles of an extracellular matrix (ECM) receptor and ECM processing enzymes in demyelinating canine distemper

S Alldinger1, S Gröters, Q Miao

  • 1Institut für Pathologie, Stiftung Tierärztliche Hochschule Hannover, Hannover, Germany. Susanne.Alldinger@tiho-hannover.de

DTW. Deutsche Tierarztliche Wochenschrift
|May 24, 2006
PubMed

Insights

Canine distemper encephalitis (CDE) involves CD44 antigen and matrix metalloproteinases (MMPs) in demyelination. These molecules may initiate and perpetuate inflammation and lesion progression in this canine model of multiple sclerosis.

Area of Science:

  • Neuroscience
  • Immunology
  • Veterinary Pathology

Background:

  • Canine distemper virus (CDV) causes central nervous system (CNS) demyelination in dogs, creating a model for human demyelinating diseases like multiple sclerosis.
  • CD44 antigen (CD44), a receptor for hyaluronate, and extracellular matrix (ECM) processing enzymes (MMPs) and their inhibitors (TIMPs) are implicated in demyelination pathogenesis.

Purpose of the Study:

  • To review the role of CD44, MMPs, and TIMPs in the pathogenesis of demyelination in canine distemper encephalitis (CDE).
  • To elucidate the involvement of these molecules in both acute and chronic stages of CDE.

Main Methods:

  • Review of existing literature on CD44, MMPs, and TIMPs in canine distemper encephalitis.
  • Analysis of CD44, MMP, and TIMP expression patterns in acute, subacute, and chronic CDE lesions.
  • Correlation of molecular expression with neuropathological changes, including astrocyte activation and immune cell infiltration.

Main Results:

  • CD44 up-regulation and astrocyte activation are observed in acute/subacute CDE, paralleled by increased MMPs and TIMPs, primarily in astrocytes and microglia.
  • In chronic CDE lesions, CD44 expression decreases with fewer GFAP-positive astrocytes, but CD44 is found on perivascular mononuclear cells.
  • MMP and TIMP expression generally decreases in chronic lesions, except for MMP-11, -12, and -13.

Conclusions:

  • CD44 and MMPs are potentially involved in initiating demyelination and ECM disturbances in CDE.
  • CD44 ligation in early stages may trigger inflammatory responses via chemokines and cytokines.
  • An MMP-TIMP imbalance in chronic CDE might drive lesion progression, accompanied by CD44-positive immune cell influx.

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