Please use this identifier to cite or link to this item: https://doi.org/10.7150/thno.81583
Title: Colonization with two different Blastocystis subtypes in DSS-induced colitis mice is associated with strikingly different microbiome and pathological features
Authors: Deng, Lei
Wojciech, Lukasz 
Png, Chin Wen 
Kioh, Dorinda Yan Qin 
Gu, Yuxiang
Aung, Thet Tun 
Malleret, Benoit 
Chan, Eric Chun Yong 
Peng, Guangneng
Zhang, Yongliang 
Gascoigne, Nicholas Robert John 
Tan, Kevin Shyong Wei 
Keywords: Blastocystis
Gut microbiota
IBD
DSS-induced colitis
Short-chain fatty acids
Issue Date: 1-Jan-2023
Publisher: IVYSPRING INT PUBL
Citation: Deng, Lei, Wojciech, Lukasz, Png, Chin Wen, Kioh, Dorinda Yan Qin, Gu, Yuxiang, Aung, Thet Tun, Malleret, Benoit, Chan, Eric Chun Yong, Peng, Guangneng, Zhang, Yongliang, Gascoigne, Nicholas Robert John, Tan, Kevin Shyong Wei (2023-01-01). Colonization with two different Blastocystis subtypes in DSS-induced colitis mice is associated with strikingly different microbiome and pathological features. THERANOSTICS 13 (3) : 1165-1179. ScholarBank@NUS Repository. https://doi.org/10.7150/thno.81583
Abstract: Rationale: The gut microbiota plays a significant role in the pathogenesis of inflammatory bowel disease (IBD). However, the role of Blastocystis infection and Blastocystis-altered gut microbiota in the development of inflammatory diseases and their underlying mechanisms are not well understood. Methods: We investigated the effect of Blastocystis ST4 and ST7 infection on the intestinal microbiota, metabolism, and host immune responses, and then explored the role of Blastocystis-altered gut microbiome in the development of dextran sulfate sodium (DSS)-induced colitis in mice. Results: This study showed that prior colonization with ST4 conferred protection from DSS-induced colitis through elevating the abundance of beneficial bacteria, short-chain fatty acid (SCFA) production and the proportion of Foxp3+ and IL-10-producing CD4+ T cells. Conversely, prior ST7 infection exacerbated the severity of colitis by increasing the proportion of pathogenic bacteria and inducing pro-inflammatory IL-17A and TNF-α-producing CD4+ T cells. Furthermore, transplantation of ST4- and ST7-altered microbiota resulted in similar phenotypes. Conclusions: Our data showed that ST4 and ST7 infection exert strikingly differential effects on the gut microbiota, and these could influence the susceptibility to colitis. ST4 colonization prevented DSS-induced colitis in mice and may be considered as a novel therapeutic strategy against immunological diseases in the future, while ST7 infection is a potential risk factor for the development of experimentally induced colitis that warrants attention.
Source Title: THERANOSTICS
URI: https://scholarbank.nus.edu.sg/handle/10635/238423
ISSN: 1838-7640
DOI: 10.7150/thno.81583
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