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Blastocystis  is an emerging protistan parasite colonizing the human intestine. It is frequently reported to cause general intestinal symptoms of vomiting, diarrhea, and abdominal pain. We recently demonstrated that  Blastocystis  rearranged cytoskeletal proteins and induced intestinal epithelial barrier compromise. The effect of  Blastocystis  on enterocyte apoptosis is unknown, and a possible link between microbially induced enterocyte apoptosis and increased epithelial permeability has yet to be determined. The aim of this study is to assess if  Blastocystis  induces human enterocyte apoptosis and whether this effect influences human intestinal epithelial barrier function. Monolayers of polarized human colonic epithelial cell-line Caco-2 were incubated with  Blastocystis  subtype 7 and subtype 4. Assays for both early and late markers of apoptosis, phosphatidylserine externalization, and nuclear fragmentation, respectively, showed that  Blastocystis  ST-7, but not ST-4, significantly increased apoptosis in enterocytes, suggesting that  Blastocystis  exhibits host specificity and strain-to-strain variation in pathogenicity. ST-7 also activated Caco-2 caspases 3 and 9 but not 8. ST-7 induced changes in epithelial resistance, permeability, and tight junction (ZO-1) localization. Pretreatment of Caco-2 monolayers with a pan-caspase inhibitor z-VAD-fmk significantly inhibited these changes. This suggests a role for enterocyte apoptosis in   Blastocystis -mediated epithelial barrier compromise in the human intestine.

biomed research international

Strain-Dependent Induction of Human Enterocyte Apoptosis by<i>Blastocystis</i>Disrupts Epithelial Barrier and ZO-1 Organization in a Caspase 3- and 9-Dependent Manner

Strain-Dependent Induction of Human Enterocyte Apoptosis byBlastocystisDisrupts Epithelial Barrier and ZO-1 Organization in a Caspase 3- and 9-Dependent Manner