Anti-inflammatory and immunomodulatory potential of human immunoglobulin applied intrathecally in Lewis rat experimental autoimmune neuritis

- Intrathecal immunoglobulins (Ig) access the main site of inflammation in EAN.
- Intrathecal Ig ameliorates clinical signs in Lewis rats neuritis model.
- It reduces autoimmune inflammation, demyelination and complement activation.
- In a preventive concent at low concentrations it induces a Th2 cytokine shift.
- Intrathecal Ig could be a novel treatment option for autoimmune neuropathies.

Intravenous human immunoglobulins dominate in the treatment of autoimmune neuropathies. We introduce intrathecal application as a new option for experimental autoimmune neuritis in Lewis rats. After immunisation with neuritogenic P2 peptide, we show a therapeutic and preventive effect of intrathecal human immunoglobulins (5-40 mg/kg) on clinical and electrophysiological neuritis signs. Histology corroborated a lower degree of inflammation, demyelination, ICAM-1-dependent blood-nerve-barrier permeability and complement activation in the sciatic nerve. After preventive application, immunoglobulins induced a Th2 cytokine shift in the peripheral nerves already before clinical neuritis signs. Intrathecal immunoglobulin application could be a novel immunomodulatory option for autoimmune neuropathies.

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