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Blastocystis ratti induces contact-independent apoptosis, F-actin rearrangement, and barrier function disruption in IEC-6 cells

Puthia, Manoj K LU ; Sio, Selena W S ; Lu, Jia and Tan, Kevin S W (2006) In Infection and Immunity 74(7). p.23-4114
Abstract

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... (More)

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.

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author
; ; and
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Actins/metabolism, Animals, Apoptosis/physiology, Blastocystis/physiology, Cell Communication/immunology, Cell Line, Cell Membrane Permeability/physiology, Electric Impedance, Epithelial Cells/metabolism, Rats
in
Infection and Immunity
volume
74
issue
7
pages
10 pages
publisher
American Society for Microbiology
external identifiers
  • pmid:16790785
  • scopus:33745621916
ISSN
0019-9567
DOI
10.1128/IAI.00328-06
language
English
LU publication?
no
id
dac58986-d61a-4e83-b591-a6b6b130f243
alternative location
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1489721/
date added to LUP
2018-08-27 13:49:05
date last changed
2024-04-01 09:27:03
@article{dac58986-d61a-4e83-b591-a6b6b130f243,
  abstract     = {{<p>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.</p>}},
  author       = {{Puthia, Manoj K and Sio, Selena W S and Lu, Jia and Tan, Kevin S W}},
  issn         = {{0019-9567}},
  keywords     = {{Actins/metabolism; Animals; Apoptosis/physiology; Blastocystis/physiology; Cell Communication/immunology; Cell Line; Cell Membrane Permeability/physiology; Electric Impedance; Epithelial Cells/metabolism; Rats}},
  language     = {{eng}},
  number       = {{7}},
  pages        = {{23--4114}},
  publisher    = {{American Society for Microbiology}},
  series       = {{Infection and Immunity}},
  title        = {{Blastocystis ratti induces contact-independent apoptosis, F-actin rearrangement, and barrier function disruption in IEC-6 cells}},
  url          = {{http://dx.doi.org/10.1128/IAI.00328-06}},
  doi          = {{10.1128/IAI.00328-06}},
  volume       = {{74}},
  year         = {{2006}},
}