2018年7月
The effect of lactoferrin and pepsin-treated lactoferrin on IEC-6 cell damage induced by clostridium difficile toxin B
Shock
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- 巻
- 50
- 号
- 1
- 開始ページ
- 119
- 終了ページ
- 125
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1097/SHK.0000000000000990
- 出版者・発行元
- LIPPINCOTT WILLIAMS & WILKINS
Clostridium difficile infections (CDI) have recently increased worldwide. Some CDI progress to fulminant and recurrent CDI and are associated with high mortality and morbidity. CD produces toxins A and B, which cause intestinal mucosal damage, although toxin B exhibits greater cytotoxicity. Pepsin-treated lactoferrin (PLF) is the decomposed product of lactoferrin (LF), a multifunctional glycoprotein with anti-inflammatory properties. Here, we investigate the effects of LF and PLF in toxin B-stimulated rat intestinal epithelial (IEC-6) cells. Different toxin B concentrationswere added to IEC-6 cells with or without LF or PLF. Mitochondrial function and cell cytotoxicity were assessed by measuring WST-1 and LDH levels, respectively. WST-1 levels were higher in IEC-6 cells treated with toxin B and LF or PLF than in the toxin B-only control (P<0.05). Compared with the toxin B-only control, LDH levels significantly decreased after toxin B and LF or PLF addition (P<0.05). Wound restitution measurement using microscopy demonstrated significantly greater levels of wound restitution in cells treated with toxin B and LF or PLF than in those treated with toxin B alone after 12 h (P<0.001). Furthermore, changes in IEC-6 cell tight junctions (TJs) were evaluated by immunofluorescence microscopy and zonula occludens-1 (ZO1) protein expression. When LF or PLF were added to IEC-6 cells, TJ structures were maintained, and ZO-1 and occludin expression was upregulated. Taken together, these results demonstrate that LF and PLF prevent the cytotoxicity of toxin B and might have the potential to control CDI.
- リンク情報
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- DOI
- https://doi.org/10.1097/SHK.0000000000000990
- Web of Science
- https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000441344700017&DestApp=WOS_CPL
- URL
- http://journals.lww.com/shockjournal/Fulltext/10.1097/SHK.0000000000000990
- ID情報
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- DOI : 10.1097/SHK.0000000000000990
- ISSN : 1073-2322
- eISSN : 1540-0514
- Web of Science ID : WOS:000441344700017