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Early changes in experimental allergic neuritis.

H C Powell, S L Braheny, R R Myers

    Laboratory Investigation; a Journal of Technical Methods and Pathology
    |March 1, 1983
    PubMed
    Summary
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    In experimental allergic neuritis, increased vascular permeability is the first sign, leading to edema, inflammation, and elevated endoneurial fluid pressure (EFP) in rat sciatic nerves.

    Area of Science:

    • Neuroscience
    • Immunology
    • Pathology

    Background:

    • Experimental allergic neuritis (EAN) is an animal model for inflammatory neuropathies.
    • Edema and elevated endoneurial fluid pressure (EFP) are characteristic of EAN.

    Purpose of the Study:

    • To investigate the temporal sequence of morphologic changes in EAN.
    • To correlate changes in vascular permeability, edema, and EFP during EAN development.

    Main Methods:

    • Lewis rats were inoculated with peripheral nerve emulsion to induce EAN.
    • Endoneurial fluid pressure (EFP) was measured serially (6-21 days post-inoculation).
    • Horseradish peroxidase leakage, histology, and immunoperoxidase staining were used to assess vascular permeability, edema, and immunoglobulin deposition.

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    Main Results:

    • Altered vascular permeability, evidenced by horseradish peroxidase leakage, occurred by 10 days post-inoculation.
    • EFP elevation was observed after 11 days, peaking between 12-16 days.
    • Severe endoneurial edema, inflammatory cell infiltration, mast cell degranulation, and subperineurial immunoglobulin deposition were noted from 12 days onwards.

    Conclusions:

    • Altered vascular permeability is the earliest morphologic change in EAN.
    • This is followed by antibody-containing edema fluid accumulation, inflammatory cell infiltration, and increased EFP.
    • The findings elucidate the pathogenic cascade in experimental allergic neuritis.