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Infection and Immunity, July 2006, p. 4114-4123, Vol. 74, No. 7
0019-9567/06/$08.00+0     doi:10.1128/IAI.00328-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Blastocystis ratti Induces Contact-Independent Apoptosis, F-Actin Rearrangement, and Barrier Function Disruption in IEC-6 Cells

Manoj K. Puthia,1,2 Selena W. S. Sio,1 Jia Lu,2 and Kevin S. W. Tan1*

Laboratory of Molecular and Cellular Parasitology, Department of Microbiology, Yong Loo Lin School of Medicine, National University of Singapore, 5 Science Drive 2, Singapore 117597, Singapore,1 Defence Medical and Environmental Research Institute, DSO National Laboratories, 27 Medical Drive, DSO (Kent Ridge), Singapore 117510, Singapore2

Received 28 February 2006/ Returned for modification 22 April 2006/ Accepted 25 April 2006

Blastocystis is an enteric protozoan purportedly associated with numerous clinical cases of diarrhea, flatulence, vomiting, and other gastrointestinal symptoms. Despite new knowledge of Blastocystis cell biology, genetic diversity, and epidemiology, its pathogenic potential remains controversial. Numerous clinical and epidemiological studies either implicate or exonerate the parasite as a cause of intestinal disease. Therefore, the aim of this study was to investigate the pathogenic potential of Blastocystis by studying the interactions of Blastocystis ratti WR1, an isolate of zoonotic potential, with a nontransformed rat intestinal epithelial cell line, IEC-6. Here, we report that B. ratti WR1 induces apoptosis in IEC-6 cells in a contact-independent manner. Furthermore, we found that B. ratti WR1 rearranges F-actin distribution, decreases transepithelial resistance, and increases epithelial permeability in IEC-6 cell monolayers. In addition, we found that the effects of B. ratti on transepithelial electrical resistance and epithelial permeability were significantly abrogated by treatment with metronidazole, an antiprotozoal drug. Our results suggest for the first time that Blastocystis-induced apoptosis in host cells and altered epithelial barrier function might play an important role in the pathogenesis of Blastocystis infections and that metronidazole has therapeutic potential in alleviating symptoms associated with Blastocystis.

* Corresponding author. Mailing address: Laboratory of Molecular and Cellular Parasitology, Department of Microbiology, Yong Loo Lin School of Medicine, National University of Singapore, 5 Science Drive 2, Singapore 117597, Singapore. Phone: (65) 6516 6780. Fax: (65) 6776 6872. E-mail: mictank{at}nus.edu.sg.

Editor: W. A. Petri, Jr.

Infection and Immunity, July 2006, p. 4114-4123, Vol. 74, No. 7
0019-9567/06/$08.00+0     doi:10.1128/IAI.00328-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Tan, K. S. W. (2008). New Insights on Classification, Identification, and Clinical Relevance of Blastocystis spp.. Clin. Microbiol. Rev. 21: 639-665 [Abstract] [Full Text]  
  • Lantsman, Y., Tan, K. S. W., Morada, M., Yarlett, N. (2008). Biochemical characterization of a mitochondrial-like organelle from Blastocystis sp. subtype 7. Microbiology 154: 2757-2766 [Abstract] [Full Text]  
  • Puthia, M. K., Lu, J., Tan, K. S. W. (2008). Blastocystis ratti Contains Cysteine Proteases That Mediate Interleukin-8 Response from Human Intestinal Epithelial Cells in an NF-{kappa}B-Dependent Manner. Eukaryot Cell 7: 435-443 [Abstract] [Full Text]  


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