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sICAM-1 in meningoencephalitis due to Angiostrongylus cantonensis

Alberto Juan Dorta-Contreras1, Piotr Lewczuc, Elena Noris-García

  • 1Laboratorio Central Liquido Cefalorraquideo (LABCEL), Ciudad de La Habana, Cuba. adorta@infomed.sld.cu

Arquivos De Neuro-Psiquiatria
|November 23, 2006
PubMed

Insights

Eosinophilic meningoencephalitis in children caused by Angiostrongylus cantonensis shows increased CSF protein and albumin. Soluble intercellular adhesion molecule-1 (sICAM-1) dynamics may indicate disease progression and regulate inflammation.

Area of Science:

  • Neurology
  • Infectious Diseases
  • Parasitology

Background:

  • Angiostrongylus cantonensis causes eosinophilic meningoencephalitis, an emerging disease in the Americas.
  • This parasitic infection affects the central nervous system, particularly in pediatric populations.

Purpose of the Study:

  • To investigate the clinical and laboratory findings in children with Angiostrongylus cantonensis meningoencephalitis.
  • To evaluate the role of soluble intercellular adhesion molecule-1 (sICAM-1) in the pathogenesis and immune response of this condition.

Main Methods:

  • Studied twelve children (6-10 years old) diagnosed with eosinophilic meningoencephalitis.
  • Collected cerebrospinal fluid (CSF) and serum samples for routine analysis, protein, albumin, and sICAM-1 levels.
  • Assessed intrathecal immunoglobulin synthesis and calculated CSF/serum albumin and sICAM-1 ratios.

Main Results:

  • All patients exhibited elevated CSF total protein and Q (CSF/serum) albumin, with CSF eosinophilia.
  • No intrathecal immunoglobulin synthesis was detected.
  • Mean serum and CSF sICAM-1 levels were 337.4 ng/mL and 3.97 ng/mL, respectively. Mean Qalbumin and QsICAM-1 were 4.1 and 6.2.
  • An increased brain-derived fraction of sICAM-1 was observed in 50% of patients.

Conclusions:

  • The dynamic of the brain-derived sICAM-1 fraction may correlate with the immune response during the disease's evolution.
  • sICAM-1 might act as a negative feedback agent, controlling eosinophil migration across the blood-CSF barrier into the inflamed brain.
Abstract

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