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A role for antimicrobial peptides in intestinal microsporidiosis

Published online by Cambridge University Press:  12 December 2008

G. J. LEITCH*
Affiliation:
The Whitney Laboratory for Marine Bioscience, University of Florida, St Augustine, Florida, USA
C. CEBALLOS
Affiliation:
The Whitney Laboratory for Marine Bioscience, University of Florida, St Augustine, Florida, USA
*
*Corresponding author: The Whitney Laboratory for Marine Bioscience, University of Florida, 9505 Ocean Shore Blvd., St Augustine, FL 32080, USA. Tel: +904 461 4000. Fax: +904 461 4052. E-mail: leitch@whitney.ufl.edu

Summary

Clinical isolates from 3 microsporidia species, Encephalitozoon intestinalis and Encephalitozoon hellem, and the insect parasite Anncaliia (Brachiola, Nosema) algerae, were used in spore germination and enterocyte-like (C2Bbe1) cell infection assays to determine the effect of a panel of antimicrobial peptides. Spores were incubated with lactoferrin (Lf), lysozyme (Lz), and human beta defensin 2 (HBD2), human alpha defensin 5 (HD5), and human alpha defensin 1 (HNP1), alone and in combination with Lz, prior to germination. Of the Encephalitozoon species only E. hellem spore germination was inhibited by HNP1, while A. algerae spore germination was inhibited by Lf, HBD2, HD5 and HNP1, although HBD2 and HD5 inhibition required the presence of Lz. The effects of HBD2 and HD5 on microsporidia enterocyte infection paralleled their effects on spore germination. Lysozyme alone only inhibited infection with A. algerae, while Lf inhibited infection by E. intestinalis and A. algerae. HNP1 significantly reduced enterocyte infection by all 3 parasite species and a combination of Lf, Lz and HNP1 caused a further reduced infection with A. algerae. These data suggest that intestinal antimicrobial peptides contribute to the defence of the intestine against infection by luminal microsporidia spores and may partially determine which parasite species infects the intestine.

Type
Research Article
Copyright
Copyright © 2008 Cambridge University Press

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