Why cornea is selectively at risk for
Acanthamoeba infection is unclear. In vitro, pathogenic strains of
Acanthamoebae adhere to and produce CPEs on host cells derived not only from cornea but also from a variety of nonocular tissues (e.g., kidney, brain, ovary, esophagus, and bone)
16 17 18 19 20 21 that, in healthy, immunocompetent persons, are resistant to infection by
Acanthamoeba. This suggests that protective factors must be present in vivo, most notably in mucosal secretions such as tear fluid, saliva, and breast milk. In fact, normal human tears, saliva, and milk contain
Acanthamoeba-specific IgA antibodies capable of inhibiting the adhesion of the parasites to host cells
22 23 24 25 (Panjwani et al., unpublished observations, 2006), a key first step in the pathogenesis of infection. Thus far, secretory IgA (sIgA) antibody is the only recognized component that is widely thought to account for the protection afforded by mucosal secretions. A recent study
26 in our laboratory revealed that IgA-depleted tears of healthy persons also inhibit
Acanthamoeba-induced CPE, albeit with a lower potency than total tears. In that study, because of the limited availability of tears, it was not possible to characterize the mechanism by which the IgA-depleted tears inhibit the ameba-induced CPE. Clearly, in-depth studies requiring large quantities of starting material for characterization of the CPE-inhibiting factors will have to rely on mucosal secretions such as milk, which is clean, uncontaminated, and readily available in large quantities. Ocular tears and breast milk share many components, and, indeed, important lessons about the protective role of tear fluid have been learned from in-depth investigations on milk. In the present study, using milk as a model, we demonstrated that human mucosal secretions have the potential to provide protection against
Acanthamoeba-induced CPE by an additional mechanism that is independent of IgA and that involves the inhibition of cytotoxic proteinases of amebae.