Initial events in the breakthrough of the epithelial barrier of the small intestine by Angiostrongylus cantonensis
Although the third-stage larvae of Angiostrongylus cantonensis (AcL3) are thought to initiate infection by penetrating the epithelium of the small intestine, the mode of intestinal invasion remains obscure. Considering the inaccessibility of the gut tract and the need to sacrifice animals f...
Main Authors: | , , , , , , , , |
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Format: | Article |
Language: | English |
Published: |
University of Belgrade, University of Novi Sad
2016-01-01
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Series: | Archives of Biological Sciences |
Subjects: | |
Online Access: | http://www.doiserbia.nb.rs/img/doi/0354-4664/2016/0354-46641600029L.pdf |
Summary: | Although the third-stage larvae of Angiostrongylus cantonensis (AcL3) are
thought to initiate infection by penetrating the epithelium of the small
intestine, the mode of intestinal invasion remains obscure. Considering the
inaccessibility of the gut tract and the need to sacrifice animals for this
type of study, we devised an in vitro cell-parasite co-culture system to
examine the initial cellular and molecular events between AcL3 and host
epithelia. No apoptosis augmentation was detected in enterocytes after
introduction of larvae. A significant increase in dead cells was detected in
IEC-6, NCM460 and 293T after incubating for 4 h, with AcL3 wounding rat small
intestinal epithelial cells IEC-6 more rapidly. Under a scanning electron
microscope (SEM), cell gap opening was visualized in the IEC-6 monolayer
treated with AcL3. Loosening of the extracellular matrix (ECM) of the
monolayer was found to be involved in the parasite-cell interactions.
Pretreating the AcL3 with a protease inhibitor attenuated its penetration
ability of the artificial intestine barrier. In conclusion, AcL3 broke
through the intestinal barrier of the host with the assistance of mechanical
injury and the opening of a cell gap, but without causing apoptosis. The
interaction platform presented here may provide direct insight into the
cellular and molecular events during worm invasion of host enterocytes. |
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ISSN: | 0354-4664 1821-4339 |