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A more recent version of this article appeared on November 1, 2007

Published online before print September 6, 2007
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Copyright © 2007 American Society for Investigative Pathology
American Journal of Pathology, doi:10.2353/ajpath.2007.070147

Accepted for publication July 23, 2007.

Article

Targeting Inflammatory Demyelinating Lesions to Sites of Wallerian Degeneration

Ikuo Tsunoda*, Tomoko Tanaka*, Yukio Saijoh{dagger}, and Robert S. Fujinami*@

From the Department of Neurology*and the Program in Human Molecular Biology and Genetics,{dagger} the Eccles Institute of Human Genetics, University of Utah School of Medicine, Salt Lake City, Utah

@ To whom correspondence should be addressed. E-mail: robert.fujinami{at}hsc.utah.edu.


  Abstract

In Theiler's murine encephalomyelitis virus (TMEV) infection, an animal model for multiple sclerosis (MS), axonal injury precedes inflammatory demyelinating lesions, and the distribution of axonal damage present during the early phase of infection corresponds to regions where subsequent demyelination occurs during the chronic phase. We hypothesized that axonal damage recruits inflammatory cells to sites of Wallerian degeneration, leading to demyelination. Three weeks after TMEV infection, axonal degeneration was induced in the posterior funiculus of mice by injecting the toxic lectin Ricinus communis agglutinin (RCA) I into the sciatic nerve. Neuropathology was examined 1 week after lectin injection. Control mice, infected with TMEV but receiving no RCA I, had inflammatory demyelinating lesions in the anterior/lateral funiculi. Other control mice that received RCA I alone did not develop inflammatory lesions. In contrast, RCA I injection into TMEV-infected mice induced lesions in the posterior funiculus in addition to the anterior/lateral funiculi. We found no differences in lymphoproliferative responses or antibody titers against TMEV among the groups. This suggests that axonal degeneration contributes to the recruitment of inflammatory cells into the central nervous system by altering the local microenvironment. In this scenario, lesions develop from the axon (inside) to the myelin (outside) (Inside-Out model).




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Copyright © 2007 by the American Society for Investigative Pathology.