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Chandrassegar Saravanan1, Zhiyi Cao, Janardan Kumar

  • 1Department of Anatomy and Cell Biology, Sackler School of Graduate Biomedical Sciences, Tufts University School of Medicine, Boston, MA 02111, USA.

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Human mucosal secretions, like breast milk, protect against Acanthamoeba keratitis (AK) by inhibiting parasite-induced damage. This protection is independent of IgA antibodies and involves blocking harmful amebic proteinases.

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Area of Science:

  • Ophthalmology
  • Microbiology
  • Immunology

Background:

  • Acanthamoeba keratitis (AK) is a severe eye infection.
  • Acanthamoeba-specific IgA antibodies in mucosal secretions are thought to prevent AK by inhibiting parasite adhesion.
  • The potential for additional protective mechanisms in mucosal secretions remains unexplored.

Purpose of the Study:

  • To investigate if human mucosal secretions offer protection against Acanthamoeba-induced cytopathic effect (CPE) through mechanisms beyond IgA.
  • To identify components within mucosal secretions responsible for this IgA-independent protection.

Main Methods:

  • Breast milk served as a model for human mucosal secretions.
  • In vitro cytopathic effect (CPE) assays were performed on IgA-depleted milk and milk fractions.
  • Zymography was used to assess the activity of amebic proteinases.

Main Results:

  • IgA-depleted milk demonstrated a dose-dependent inhibition of Acanthamoeba-induced CPE.
  • Gel filtration separated milk proteins into fractions; fraction F3 exhibited significant CPE inhibitory activity.
  • Fraction F3, unlike other fractions, also inhibited amebic proteinases, which are known to cause Acanthamoeba CPE.

Conclusions:

  • Human mucosal secretions provide protection against Acanthamoeba-induced CPE via an IgA-independent pathway.
  • This protective mechanism involves the inhibition of cytotoxic amebic proteinases.
  • These findings suggest a novel therapeutic target for Acanthamoeba keratitis.